This is a beginning to intermediate level course. After completing this course, mental health professionals will be able to:
The materials in this course are based on the most accurate information available to the author at the time of writing. The field of ADHD grows daily, and new information may emerge that supersedes these course materials. This course will equip clinicians to have a basic understanding of the nature of ADHD, the history of the disorder, its causes, and its associated disorders and impairments.
This course provides an overview of the nature of Attention Deficit Hyperactivity Disorder, briefly considers its history, describes its developmental course and outcomes, and discusses its causes. Current critical issues related to these matters will be raised along the way. Given the thousands of scientific papers on this topic, this course must, of necessity, concentrate on the most important topics in this literature. Readers interested in more detail can pursue other sources (Accardo, Blondis, Whitman, & Stein, 2001; Barkley, 2006, 2011a; Barkley, Murphy, & Fischer, 2008). The author’s theoretical model of executive functioning (Barkley, 2012) and its application to ADHD also will be presented, providing a more parsimonious accounting of the many cognitive and social deficits in the disorder which points to numerous promising directions for future research while rendering a deeper appreciation for the developmental significance and seriousness of ADHD. This theory shows that ADHD involves more than just attention deficits – it also comprises central problems with inhibition, self-regulation, and the cross-temporal organization of social behavior, the phenotypic effects of which radiate outward to impact various zones of social, educational, and occupational functioning.
(This course was initially adapted with permission from the chapter by R. A. Barkley on ADHD in the text by E. J. Mash and R. A. Barkley (2002), Child Psychopathology (2nd ed.). New York: Guilford Publications, Guilford.com). It has since been updated most recently in January 2013.
Literary references to individuals having serious problems with inattention, hyperactivity, and poor impulse control date back to Shakespeare, who made reference to a malady of attention in King Henry VIII. A hyperactive child was the focus of a German poem, “Fidgety Phil,” by physician, Heinrich Hoffman (see Stewart, 1970). William James (1890), in his Principles of Psychology, described a normal variant of character that he called the “explosive will” that resembles the difficulties experienced by those who today are called ADHD. But, the first paper in the medical literature on disorders of attention such as ADHD is a short chapter on this topic in a medical textbook (initially published anonymously) by Melchior Adam Weikard in 1775 (Barkley & Peters, 2012). Weikard was a prominent German physician who described symptoms of distractibility, poor persistence, impulsive actions, and inattention more generally quite similar to the symptoms used today to describe the inattention associated with ADHD. This text was followed by that of the Scottish physician Alexander Crichton in 1798, who provided even more detailed descriptions of this sort of inattention as well as identifying a second disorder of attention thought to involve low power to focus attention (Palmer & Finger, 2001). Further serious clinical interest in ADHD did not occur again until the appearance of three lectures by the English physician George Still (1902) before the Royal Academy of Physicians.
Still reported on a group of 20 children in his clinical practice whom he defined as having a deficit in “volitional inhibition” (p. 1008) that led to a “defect in moral control” (p. 1009) over their own behavior. Described as aggressive, passionate, lawless, inattentive, impulsive, and overactive, many of these children today would be diagnosed not only as ADHD but also as having oppositional defiant disorder (ODD). Still’s observations were quite astute, describing many of the associated features of ADHD that would come to be corroborated in research over the next century: (1) an overrepresentation of male subjects (ratio of 3:1 in Still’s sample); (2) high comorbidity with antisocial conduct and depression; (3) an aggregation of alcoholism, criminal conduct, and depression among the biological relatives; (4) a familial predisposition to the disorder, likely of hereditary origin; (5) yet with the possibility of the disorder also arising from acquired injury to the nervous system.
Interest in these children arose in North America around the time of the great encephalitis epidemics of 1917-1918. Children surviving these brain infections had many behavioral problems similar to those comprising contemporary ADHD (Ebaugh, 1923; Hohman, 1922; Stryker, 1925). These cases and others known to have arisen from birth trauma, head injury, toxin exposure, and infections (see Barkley, 2006) gave rise to the concept of a brain-injured child syndrome (Strauss & Lehtinen, 1947), often associated with mental retardation, that would eventually become applied to children manifesting these same behavior features but without evidence of brain damage or retardation (Dolphin & Cruickshank, 1951; Strauss & Kephardt, 1955). This concept evolved into that of minimal brain damage, and eventually minimal brain dysfunction (MBD), as challenges were raised to the original label in view of the dearth of evidence of obvious brain injury in most cases (see Kessler, 1980, for a more detailed history of MBD).
By the 1950s-1970s, focus shifted away from etiology and toward the more specific behavior of hyperactivity and poor impulse control characterizing these children, reflected in labels such as “hyperkinetic impulse disorder” or “hyperactive child syndrome” (Burks, 1960; Chess, 1960). The disorder was thought to arise from cortical overstimulation due to poor thalamic filtering of stimuli entering the brain (Knobel, Wolman, & Mason, 1959; Laufer, Denhoff, & Solomons, 1957). Despite a continuing belief among clinicians and researchers of this era that the condition had some sort of neurological origin, the larger influence of psychoanalytic thought held sway. And so, when the second edition of Diagnostic and Statistical Manual of Mental Disorders (DSM-II) appeared, all childhood disorders were described as “reactions,” and the hyperactive child syndrome became “hyperkinetic reaction of childhood” (American Psychiatric Association, 1968).
The recognition that the disorder was not caused by brain damage seemed to follow a similar argument made somewhat earlier by the prominent child psychiatrist Stella Chess (1960). It set off a major departure between professionals in North America and those in Europe that continues, to a lessening extent, to the present. Europe continued to view hyperkinesis for most of the latter half of the 20th century as a relatively rare condition of extreme overactivity often associated with mental retardation or evidence of organic brain damage. This discrepancy in perspectives has been converging over the last decades as is evident in the similarity of the DSM-IV criteria (see below) with those of ICD-10 (World Health Organization, 1994). Nevertheless, the manner in which clinicians and educators view the disorder remains quite disparate; in North America, Canada, and Australia, such children have ADHD, a developmental disorder, whereas in Europe they are viewed as having conduct problem or disorder, a behavioral disturbance believed to arise largely out of family dysfunction and social disadvantage.
By the 1970s, research emphasized the problems with sustained attention and impulse control in addition to hyperactivity (Douglas, 1972). Douglas (1980, 1983) theorized that the disorder had four major deficits: (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’s emphasis on attention along with the numerous studies of attention, impulsiveness, and other cognitive sequelae that followed (see Douglas, 1983; and Douglas & Peters, 1978, for reviews), eventually led to renaming the disorder as attention deficit disorder (ADD) in 1980 (DSM-III; American Psychiatric Association, 1980). Significant, historically, was the distinction in DSM-III between two types of ADD: those with hyperactivity and those without it. Little research existed at the time on the latter subtype that would have supported such a distinction being made in an official and increasingly prestigious diagnostic taxonomy. Yet, in hindsight, this bald assertion led to valuable research on the differences between these two supposed forms of ADD that otherwise would never have taken place. That research may have been fortuitous, as it may be leading to the conclusion that a subset of those having ADD without hyperactivity may actually be exhibiting a separate, distinct, and qualitatively unique disorder rather than a subtype of ADHD; one tentatively named sluggish cognitive tempo (Barkley, 2012a, 2012b; Milich, Ballantine & Lynam, 2001).
Even so, within a few years of the creation of the label ADD, concern arose that the important features of hyperactivity and impulse control were being de-emphasized when in fact they were critically important to differentiating the disorder from other conditions and to predicting later developmental risks (Barkley, 2006; Barkley et al., 2008; Weiss & Hechtman, 1993). In 1987, the disorder was renamed as attention-deficit hyperactivity disorder in DSM-III-R (American Psychiatric Association, 1987), and a single list of items incorporating all three symptoms was specified. Also important here was the placement of the condition of ADD without hyperactivity, renamed undifferentiated attention-deficit disorder, in a separate section of the manual from ADHD with the specification that insufficient research existed to guide in the construction of diagnostic criteria for it at that time.
During the 1980s, reports focused instead on problems with motivation generally, and an insensitivity to response consequences specifically (Barkley, 1989a; Glow & Glow, 1979; Haenlein & Caul, 1987). Research was demonstrating that under conditions of continuous reward, the performances of ADHD children were often indistinguishable from normal children on various lab tasks but when reinforcement patterns shifted to partial reward or to extinction (no reward) conditions, children with ADHD showed significant declines in their performance (Douglas & Parry, 1983, 1994; Parry & Douglas, 1983). It was also observed that deficits in the control of behavior by rules characterized these children (Barkley, 1989a).
Over the next decade, researchers employed information-processing paradigms to study ADHD and found that problems in perception and information processing were not so evident as were problems with motivation and response inhibition (Barkley, Grodzinsky, & DuPaul, 1992; Schachar & Logan, 1990; Sergeant, 1988; Sergeant & Scholten, 1985a, 1985b). The problems with hyperactivity and impulsivity also were found to form a single dimension of behavior (Achenbach & Edelbrock, 1983; Goyette, Conners, & Ulrich, 1978; Lahey et al., 1988), which others described as “disinhibition” (Barkley, 1990). All of this led to the creation of two separate, but highly correlated lists of symptoms and thresholds for ADHD when the DSM-IV was published later in the decade (American Psychiatric Association, 1994; again, in 2001); one for inattention and another for hyperactive-impulsive behavior. Unlike its predecessor, DSM-III-R, the establishment of the inattention list once again permitted the diagnosis of a subtype of ADHD that consisted principally of problems with attention (ADHD predominantly inattentive type). It also permitted, for the first time, the distinction of a subtype of ADHD that consisted chiefly of hyperactive-impulsive behavior without significant inattention (ADHD, predominantly hyperactive-impulsive type). Children having significant problems from both item lists, which constitute the majority of patients, were titled ADHD, combined type.
All this has now been superseded by the development and publication of DSM-5 (American Psychiatric Association, 2013). The DSM-5 contains several changes discussed in more detail below (see “Diagnostic Criteria and Related Issues”). Suffice to say here that while the same symptoms remain as in DSM-IV, clarifications of them for older teens and adults have been added in parentheses next to each symptom, the age of onset has been increased to age 12, a lower symptom threshold of 5 will be required for adults (instead of the traditional 6 used with children), and the subtypes are eliminated, given that research over the prior 18 years did not find them reliable, stable over development (Valo & Tannock, 2010), valid, and hence useful. ADHD is now recognized as a single disorder varying in severity across its two highly related symptom dimensions rather than comprised of three distinct types of a disorder. Clinicians will now simply specify which set of symptoms is more predominant by qualifying the diagnosis with a “presentation,” such as predominantly inattentive presentation.
Healthy debate continues to the present over the core deficit(s) in ADHD with increasing weight being given to problems with behavioral inhibition, self-regulation, and the related domain of executive functioning (Barkley, 1997a, 1997b, 2006, 2012; Nigg & Casey, 2005; Shiels & Hawk, 2010; Willcutt et al., 2010), as well as to delay aversion (difficulty waiting for events)(Coghill, 2005; Sonuga-Barke et al., 1996) and cognitive-energetic mechanisms (Sergeant, 2005). The symptoms of inattention may actually be evidence of impaired working memory and not perceptual, filtering, or selection (input) problems (Barkley, 2011a; Barkley & Murphy, 2011). Likewise, controversy continues to swirl around the place of a subtype composed primarily of a distinct form of inattention, called sluggish cognitive tempo (SCT), that is comprised of daydreaming, staring, slow processing, lethargy, and hypoactivity within the larger condition of ADHD (see Clinical Psychology: Science and Practice, 2001, Vol. 8 (4) for one of the first debates on this issue), with some arguing for it being a new, unique disorder from ADHD (Barkley, 2012a, 2012b; Carr, Henderson, & Nigg, 2010; Milich et al., 2001; Penny et al., 2010). SCT will not appear in DSM-5 given that far more research is needed on this condition in order to justify it being identified as a new psychiatric disorder. Yet research at the moment seems well on the way to eventually doing so (Barkley, 2012a, 2012b).
Research employing factor analysis has repeatedly identified two distinct behavioral dimensions underlying the various behavioral problems (symptoms) thought to characterize ADHD in children (Barkley, 2006; Burns, Boe, Walsh, Sommers-Flanagan, & Teegarden, 2001; DuPaul et al., 1997; Lahey et al., 1994; Pillow, Pelham, Hoza, Molina, & Stultz, 1998) while three factors appear to arise by adulthood (Barkley, 2011b; Barkley, Murphy, & Fischer, 2008). The two childhood dimensions have been identified across various ethnic and cultural groups, including Native American children (Beiser, Dion, & Gotowiec, 2000) and represent inattention and hyperactive-impulsive behavior. In adults, a small verbal impulsivity dimension emerges that is somewhat separable from the other two. In contrast, symptoms of SCT form a separate dimension from those of ADHD, though partially correlated with them (especially the ADHD inattention dimension) (Barkley, 2012a). This is some of the evidence used to argue that SCT is likely a distinct disorder from ADHD yet one that can be comorbid with it. Unlike ADHD, the symptoms of SCT do not appear to decline with age, have different family and demographic correlates, and manifest a different pattern of comorbidity with other psychiatric disorders in contrast to ADHD (Barkley, 2012b; Penny et al., 2010).
Attention represents a multidimensional construct (Bate, Mathias, & Crawford, 2001; Mirsky, 1996; Strauss, Thompson, Adams, Redline, & Burant, 2000) implying that several qualitatively distinct problems with attention eventually may be found (Barkley, 2001a). The dimension impaired in ADHD reflects an inability to sustain attention or persist at tasks or play activities, to remember and follow through on rules and instructions, and to resist distractions while doing so. I have elsewhere argued that this dimension more likely reflects problems with executive functioning, especially working memory than just poor attention, per se (Barkley, 1997b), and evidence is becoming available to support this contention (Barkley & Murphy, 2010; Frazier et al., 2004; Hervey et al., 2004). 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, are forgetful, and change activities more often than others (DuPaul, Powers, Anastopolous, & Reid, 1999). The same is true of adults with ADHD (Barkley, 2011a; Barkley et al., 2008). Research employing objective measures corroborates these complaints about children through observations of more “off-task” behavior, less work productivity, greater looking away from assigned tasks (including television), less persistence at tedious tasks, such as continuous performance tasks, being slower and less likely to return to an activity once interrupted, less attentiveness to changes in the rules governing a task, and being less capable of shifting attention across tasks flexibly (Borger & van der Meere, 2000; Hoza, Pelham, Waschbusch, Kipp, & Owens, 2001; Lorch et al., 2000; Luk, 1985; Newcorn et al., 2001; Seidman, Biederman, Faraone, Weber, & Ouellette, 1997; Shelton et al., , 1998). This inattentive behavior distinguishes these children from those with learning disabilities (Barkley, DuPaul, & McMurray, 1990) or other psychiatric disorders (Chang et al., 1999; Swaab-Barneveld et al., 2000) and does not appear to be a function of other disorders often comorbid with ADHD (anxiety, depression, or oppositional and conduct problems) (Barkley et al., 2008; Murphy, Barkley, & Bush, 2001; Klorman et al., 1999; Newcorn et al., 2001; Nigg, 1999; Seidman et al., 1997).
As with attention, inhibition is a multidimensional construct (Nigg, 2000; Olson, Schilling, & Bates, 1999) and thus various, qualitatively distinct forms of inhibitory impairments may eventually be found in children. The problems with inhibition seen in ADHD are thought to involve voluntary or executive inhibition of prepotent or dominant responses rather than impulsiveness that may be more motivationally controlled, as in a heightened sensitivity to available reward (reward seeking) or to excessive fear (Nigg, 2001; Nigg & Casey, 2005). Some evidence suggests that an excess sensitivity to reward or to sensation seeking may be more associated with severity of conduct disorder or psychopathy than with severity of ADHD (Beauchaine, Katkin, Strassberg, & Snarr, 2001; Dougherty & Quay, 1991; Fischer, Barkley, Smallish, & Fletcher, 2002; Matthys, van Goozen, de Vries, Cohen-Kettenis, & van Engeland, 1998). Evidence is less clear about deficits in automatic or involuntary inhibition, as in eye-blinking or negative priming, being associated with ADHD (Nigg, 2001).
More specifically, children with ADHD manifest difficulties with excessive activity level and fidgetiness, less ability to stay seated when required, greater touching of objects, moving about, running, and climbing than other children, playing noisily, talking excessively, acting impulsively, interrupting others’ activities, and being less able than others to wait in line or take turns in games (American Psychiatric Association, 1994). Parents and teachers describe them as acting as if driven by a motor, incessantly in motion, always on the go, and unable to wait for events to occur. Research objectively documents them to be more active than other children (Barkley & Cunningham, 1979a; Dane, Schachar, & Tannock, 2000; Luk, 1985; Porrino et al., 1983; Shelton et al., 1998), to have considerable difficulties with stopping an ongoing behavior (Schachar, Tannock, & Logan, 1993; Milich, Hartung, & Haigler, 1994; Nigg, 1999, 2001; Oosterlaan, Logan, & Sergeant, 1998), to talk more than others (Barkley, Cunningham, & Karlsson, 1983), to interrupt others’ conversations (Malone & Swanson, 1993), to be less able to resist immediate temptations and delay gratification (Anderson, Hinshaw, & Simmel, 1994; Barkley, Edwards, Laneiri, & Metevia, 2001; Olson et al., 1999; Rapport, Tucker, DuPaul, Merlo, & Stoner, 1986; Solanto et al., 2001), and to respond too quickly and too often when they are required to wait and watch for events to happen, as is often seen in impulsive errors on continuous performance tests (Losier, McGrath, & Klein, 1996; Newcorn et al., 2001). Although less frequently examined, the differences in activity and impulsiveness have been found between children with ADHD and those with learning disabilities (Barkley, DuPaul, & McMurray, 1990; Bayliss & Roodenrys, 2000; Klorman et al., 1999; Willcutt et al., 2001). Mounting evidence further shows that these inhibitory deficits are not merely a function of other psychiatric disorders that may overlap with ADHD (Barkley, Edwards, Laneiri, & Metevia, 2001; Halperin, Matier, Bedi, Sharpin, & Newcorn, 1992; Fischer et al., 2002; Murphy, Barkley, & Bush, 2001; Nigg, 1999; Oosterlaan et al., 1998; Seidman et al., 1997).
Interestingly, research shows that the problems with inhibition arise first (at age 3 to 4-years-old) ahead of those related to inattention (at age 5 to 7-years-old), and of those of SCT that may arise even later (ages 8 to 10-years-old) (Barkley, 2012a, 2012b; Hart et al., 1995; Loeber, Green, Lahey, Christ, & Frick, 1992; Milich et al., 2001). Whereas the symptoms of disinhibition in the DSM item lists seem to decline with age until early adulthood (age 30), perhaps owing to their heavier weighting with hyperactive than impulsive behavior, those of inattention remain relatively more stable during the elementary grades (Hart et al., 1995). But even those symptoms eventually decline by adolescence (Barkley, Fischer, Fletcher, & Smallish, 2002; Fischer, Barkley, Fletcher, & Smallish, 1993a) and further until early adulthood (Barkley et al., 2008), though not to normal levels in most cases. Why the inattention arises later than the disinhibitory symptoms and does not decline when the latter do over development remains an enigma. But it likely has to do with the fact that the inattention symptom list reflects the broader domain of executive deficits that may take more time to emerge in development yet prove highly persistent once apparent. As noted above, it could also simply reflect the different weightings of symptoms in the DSM. Those of hyperactivity may be more typical of preschool to early school-age children and are over-represented in the DSM list while those reflecting inattention may be more characteristic of school-age children and adults. Another explanation comes from the theoretical model described below (Barkley, 1997b, 2012) in which inhibition and the two types of working memory (nonverbal and verbal) emerge at separate times in development.
The symptoms comprising ADHD are greatly affected in their level of severity by a variety of situational and task-related factors (Barkley, 2006). Douglas (1972) commented on the greater variability of task performances made by ADHD compared to control children. Many others since then have found that excessive variability in behavior and task performance is commonplace in ADHD (see Douglas, 1983). The finding is especially common in measures of reaction time (Chee, Logan, Schachar, Lindsay, & Wachsmuth, 1989; Fischer et al., 2002; Kuntsi, Oosterlaan, & Stevenson, 2001; Murphy et al., 2001; Scheres, Oosterlaan, & Sergeant, 2001).
A number of other factors influence the ability of children with ADHD to sustain their attention to task performance, control their impulses to act, regulate their activity level, and/or to produce work consistently. Research dating back several decades shows that the performance of ADHD children is worse: (1) later in the day than earlier (Dane et al., 2000; Porrino et al., 1983; Zagar & Bowers, 1983); (2) in greater task complexity such that organizational strategies are required (Douglas, 1983); (3) when restraint is demanded (Barkley & Ullman, 1975; Luk, 1985); (4) under low levels of stimulation (Antrop, Roeyers, Van Oost, & Buysse, 2000; Zentall, 1985); (5) under more variable schedules of immediate consequences in the task (Carlson, Mann, & Alexander, 2000; Carlson & Tamm, 2000; Douglas & Parry, 1983, 1994; Slusarek, Velling, Bunk, & Eggers, 2001; Tripp & Alsop, 1999); (6) under longer delay periods prior to reinforcement availability (Solanto et al., 2001; Sonuga-Barke, Taylor, & Heppinstall, 1992; Tripp & Alsop, 2001); and (7) in the absence of adult supervision during task performance (Draeger, Prior, & Sanson, 1986; Gomez & Sanson, 1994).
Besides the aforementioned factors, which chiefly apply to task performance, variability has also been documented across more macroscopic settings. For instance, 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 public scrutiny (i.e., in church, in restaurants, when a parent is on the phone, etc.) than in free play situations (Altepeter & Breen, 1992; Barkley, 2012c; Barkley & Edelbrock, 1987; DuPaul & Barkley, 1992). Although they will be more disruptive when their fathers are at home than during free play, children with ADHD are still rated as much less problematic when the father is at home than in most other contexts. Fluctuations in the severity of ADHD symptoms have also been documented across a variety of school contexts (Barkley & Edelbrock, 1987; DuPaul & Barkley, 1992). In this case, contexts involving task-directed persistence and behavioral restraint (classroom) are the most problematic, with significantly fewer problems posed by contexts involving less work and behavioral restraint (i.e., at lunch, in hallways, at recess, etc.), and even fewer problems being posed during special events (i.e., field trips, assemblies, etc.) (Altepeter & Breen, 1992).
Children with ADHD often demonstrate deficiencies in many other cognitive abilities. Among these, are difficulties with: (1) physical fitness, gross and fine motor coordination, and motor sequencing (Breen, 1989; Denckla & Rudel, 1978; Harvey & Reid, 1997; Kadesjo & Gillberg, 1999; Mariani & Barkley, 1997); (2) speed of color naming (Tannock, Martinussen, & Frijters, 2000); (3) verbal and nonverbal working memory and mental computation (Barkley, 1997; Mariani & Barkley, 1997; Murphy et al., 2001; Zentall & Smith, 1993); (4) story recall (Lorch et al., 2000; Sanchez, Lorch, Milich, & Welsh, 1999); (5) planning and anticipation (Grodzinsky & Diamond, 1992; Klorman et al., 1999); (6) verbal fluency and confrontational communication (Grodzinsky & Diamond, 1992; Zentall, 1988); (5) effort allocation (Douglas, 1983; Nigg et al., 1998; Sergeant & van der Meere, 1994; Voelker, Carter, Sprague, Gdowski, & Lachar, 1989); (6) developing, applying, and self-monitoring organizational strategies (Clark et al., 2000; Hamlett, Pellegrini, & Connors, 1987; Purvis & Tannock, 1997; Zentall, 1988); (7) the internalization of self-directed speech (Berk & Potts, 1991; Copeland, 1979; Winsler, 1998; Winsler, Diaz, Atencio, McCarthy, & Chabay, 2000); (8) adhering to restrictive instructions (Danforth, Barkley, & Stokes, 1991; Roberts, 1990; Routh & Schroeder, 1976); and (9) self-regulation of emotion (Barkley, 2010; Barkley & Fischer, 2010; Barkley & Murphy, 2010; Braaten & Rosen, 2000; Maedgen & Carlson, 2000). The latter difficulties with emotional control may be especially salient in children having ADHD with comorbid oppositional defiant disorder (ODD) (Melnick & Hinshaw, 2000) and may well explain the high risk for developing ODD in most cases of ADHD (Barkley, 2010). Several studies have also demonstrated that ADHD may be associated with less mature or diminished moral development (Hinshaw, Herbsman, Melnick, Nigg, & Simmel, 1993; Nucci & Herman, 1982; Simmel & Hinshaw, 1993). Many of these cognitive difficulties appear to be specific to ADHD and are not a function of its commonly comorbid disorders, such as learning disabilities, depression, anxiety, or oppositional/conduct disorder (Barkley, Edwards, Lanieri, & Metevia, 2001; Barkley et al., 2008; Clark, Prior, & Kinsella, 2000; Klorman et al., 1999; Murphy et al., 2001; Nigg, 1999; Nigg et al., 1998).
The commonality among most or all of these seemingly disparate abilities is that all have been considered to fall within the domain of “executive functions” in the field of neuropsychology (Barkley, 1997b; , 2012d; Denckla, 1996) or “metacognition” and self-regulation in developmental psychology (Flavell, 1970; Torgesen, 1994; Welsh & Pennington, 1988; Vohs & Baumeister, 2011), or to be affected by these functions. All seem to be mediated by the frontal cortex, and particularly the prefrontal lobes (Fuster, 1997; Stuss & Benson, 1986). Executive functions have been defined as those neuropsychological processes that permit or assist with human self-regulation (Barkley, 1997b, 2001a, 2001b, 2012d), which itself has been defined as any behavior by a person that modifies the probability of a subsequent behavior by that person so as to alter the probability of a later consequence (Kanfer & Karoly, 1972). By classifying cognitive actions or thinking as private behavior, one can understand how these private self-directed, cognitive (executive) actions fall within the definition of human self-regulation – they are private behaviors (cognitive acts) that modify other behaviors so as to alter the likelihood of later consequences for the individual. And, by appreciating the role of the frontal lobes generally, and the prefrontal cortex particularly, in these executive abilities, it is easy to see why researchers have repeatedly observed that ADHD arises out of some developmental disturbance or dysfunction of this brain region (Hart et al., 2012; Levin, 1938; Mattes, 1980; Nigg, 2006; Rubia et al., 2012).
The most recent diagnostic criteria for ADHD as defined in DSM-5 (American Psychiatric Association, 2013) are not yet published. They are expected to be so by May of 2013. These diagnostic criteria are some of the most rigorous and most empirically derived criteria ever available in the history of clinical diagnosis for this disorder. They were derived from various committees of some of the leading experts in the field who worked on this and on earlier DSMs, from literature reviews of ADHD, and from an informal survey of empirically derived rating scales assessing the behavioral dimensions related to ADHD by the committee.They were also derived from statistical analyses of the results of field trials of the items conducted for DSM III-R, DSM-IV, and most recently field trials and analyses of large existing datasets conducted for DSM-5.
Despite its empirical basis and recent revision, the DSM criteria continue to have some problems. As noted earlier, evidence is mounting that the predominantly inattentive type or presentation of ADHD (ADHD-PI) may be comprised of a rather heterogeneous mix of children, many of whom are formerly Combined Types who outgrew enough hyperactive symptoms to no longer qualify for that Combined categorization. But it is becoming evident that a subset of PI cases have a qualitatively different disorder of attention and cognitive processing (Barkley, 2012a, 2012b; Milich et al., 2001). Their symptoms generally consist of problems with daydreaming, staring, mental spaciness, lethargy, hypoactivity, and sluggishness (Barkley, 2012a, 2012b; Penny et al., 2009). This subset is probably not a subtype of ADHD but may represent a separate disorder manifesting a sluggish cognitive style and selective attention deficit, having less comorbidity with oppositional and conduct disorder, having greater comorbidity with anxiety and depression, demonstrating a more passive or withdrawn pattern of social relationships, perhaps having memory retrieval problems, and, owing to their lower level of impulsiveness, probably having a different, more benign, developmental course. In agreement with Milich et al. (2001), I believe the subset having hypoactivity, lethargy, and sluggish cognitive tempo should be set aside as a separate disorder from ADHD (Barkley, 2012a, 2012b).
Are the two separate symptom lists important rather than the one combined list used in DSM-III-R? Perhaps, but this is unsure because these dimensions are highly correlated with each other (Barkley, 2011b; DuPaul et al., 1999) and also have substantial shared genetic overlap (McLoughlin et al., 2007). In the field trial for DSM-IV (Lahey et al., 1994), significant levels of inattention mainly predicted additional problems with completing homework that were not as well predicted by the hyperactive-impulsive behavior. Otherwise, the latter predicted most of the other areas of impairment studied in this field trial. Other studies find that childhood symptoms of hyperactivity are related to adverse adolescent outcomes, such as antisocial behavior, substance abuse, and school disciplinary actions, such as suspensions/expulsions (Babinski, Hartsough, & Lambert, 1999). Symptoms of inattention seem to be primarily predictive of impairment in academic achievement, particularly reading, and school performance (DuPaul, Power, Anastopoulos, & Reid, 1998; Fischer, Barkley, Fletcher, & Smallish, 1993b; Weiss & Hechtman, 1993; Rabiner, Coie, and the Conduct Problem Prevention Research Group, 2000). Severity of hyperactive-impulsive behavior is often found to be the dimension of ADHD that more strongly predicts later conduct disorder and so risk for various forms of substance use and abuse (Molina, Smith, & Pelham, 1999). A study suggests that adolescent inattention, however, may contribute further to the risk for tobacco use beyond that risk contributed by severity of conduct disorder alone (Burke, Loeber, & Lahey, 2001). For these and other reasons, DSM-5 now presents ADHD as a single disorder within the human population that can vary in severity along its two inter-related dimensions and thus accounts for some of the heterogeneity in clinical cases, with some having higher levels of one dimension than the other. These differing cases are now recognized as representing differences in “presentation” but not in typing or in the disorder itself.
Another critical issue only partially addressed in DSM-5 is how well the diagnostic thresholds set for the two symptom lists for children (#6) apply to age groups outside of those used in the earlier DSM-IV field trial (ages 4 to 16-years-old, chiefly). This concern arises out of the well-known findings that the behavioral items comprising these lists, particularly those for hyperactivity, decline significantly with age (DuPaul et al., 1998; Hart et al., 1996). Applying the same threshold across such a declining developmental slope could produce a situation where a larger percentage of young preschool aged-children (ages 2 to 3-years-old) would be inappropriately diagnosed as ADHD (false positives), whereas a smaller than expected percentage of adults would meet the criteria (false negatives). Support of just such a problem with using these criteria for adults was found in several studies (Barkley, 2011b; Barkley et al., 2008; Murphy & Barkley, 1996a) collecting norms for DSM-IV item lists on large samples of adults, ages 17 to 84-years-old. The threshold needed to place an individual at the 93rd percentile for that person’s age group declined to four of nine inattention items and five of nine hyperactive-impulsive items for ages 17 to 29-years-old, which then fell to four of nine on each list for the 30 to 49-year-old age group, then to three of nine on each list for those 50-years-old and older. Additional evidence also supports the use of a lower threshold for diagnosis with adults (typically four symptoms per list) (Barkley, 2011a; Barkley et al., 2008). For these reasons, the DSM-5 committee entertained dropping the symptom threshold to four of nine symptoms on each list but eventually settled on using five of nine, likely so as not to increase the prevalence of adult ADHD too much through these adjustments to the diagnostic criteria.
This notion of changing symptom thresholds with age raises another critical issue for developing diagnostic criteria for ADHD, and this is the appropriateness of the content of the item set for different developmental periods. Inspection of the item lists used in DSM-IV suggests that the items for inattention may have a wider developmental applicability across school-age ranges of childhood and even into adolescence and young adulthood. Those for hyperactive-impulsive behavior, in contrast, seem much more applicable to young children and less appropriate or not at all to older teens and adults. Recall from above (Hart et al., 1996) that the symptoms of inattention remain more stable across middle childhood into early adolescence, whereas those for hyperactive-impulsive behavior decline more steeply over this same course. Although this may represent a true developmental decline in the severity of the latter symptoms, and possibly in the severity and prevalence of ADHD itself, it could also represent an illusory developmental trend. That is, it might be an artifact of using more preschool focused items for hyperactivity and more school age focused items for inattention.
Barkley et al. (2008) have identified seven symptoms that are not part of DSM-IV yet are better at discriminating adults with ADHD from those with other disorders or a general population sample. Hyperactive symptoms were not helpful in such discrimination but symptoms of poor executive functioning were so. These symptoms were:
Having four of these seven symptoms was sufficient to accurately distinguish adults with ADHD from adults with other disorders and from a general community sample.
Unfortunately, the DSM-5 committee working on ADHD elected not to incorporate any new items such as those above into the ADHD symptom list, either to capture the problems with inhibition better or to provide better items for identifying adults with ADHD. Instead, the DSM-5 now has parenthetical clarifications inserted next to each of the previous 18 DSM-IV items to make them more applicable to adolescents and adults with the disorder. Time will tell if those clarifications achieve that purpose.
Also of concern was the absence of any requirement in the DSM-IV for the symptoms to be corroborated by someone that has known the patient well, such as a parent, sibling, long-time friend, or partner. In the case of adults who are self-referred to professionals, this oversight proved problematic (Barkley et al., 2008). For instance, available evidence suggests that ADHD children (Henry, Moffitt, Caspi, Langley, & Silva, 1994) and teens and young adults significantly under-report the severity of their symptoms relative to the reports of parents (Barkley, Fischer et al., 2002; Edwards, Barkley, Laneri, & Metevia, 2001; Fischer et al., 1993b; Gittelman & Mannuzza, 1986; Romano, Tremblay, Vitaro, Zoccolillo, & Pagani, 2001). This pattern continues until about age 27-30 when the reverse begins to become apparent (Barkley, Knouse, & Murphy, 2011). There is good reason that self-awareness might be limited by this disorder, at least until early adulthood (Barkley et al., 2008). For these reasons, the DSM-5 now recommends that patient self-reports be corroborated by someone who knows the patient well in making a diagnosis of ADHD at any age.
These issues are not merely academic. My colleagues and I have been involved in follow-up research with ADHD children into their adulthood and have been impressed at the chronicity of impairments created by the disorder despite an apparent decline in the percentage of cases continuing to meet diagnostic criteria and an apparent decline in the severity of the symptoms used in these criteria (Barkley, Fischer, Edelbrock, & Smallish, 1990; Barkley, Fischer, Smallish, & Fletcher, 2002; Fischer et al., 1993a). Recently, we found that if the formerly ADHD children, who are now adults, are interviewed using the DSM criteria, just 5 percent of them report sufficient symptoms to receive the diagnosis (Barkley, Fischer et al., 2002), a figure nearly identical to that for the New York longitudinal studies (Mannuzza, Klein, Bessler, Malloy, & LaPadula, 1993, 1998). If instead the parents are interviewed, this figure rises to 46% – a nine-fold difference in persistence of disorder as a function of reporting source. If instead of the recommended DSM symptom threshold, one substitutes a developmentally referenced criterion (the 98th percentile) based on same-age control adults, then 12% of the probands now have the disorder as adults based on self-reports while the figure climbs to 66% based on parental reports. Whose reports of current functioning are more valid? We addressed this by examining the relationship of self-reports and parent-reports to various domains of major life activities and outcomes (education, occupational functioning, friendships, crime, etc.). Parent reports made a substantially larger contribution to nearly all outcome domains and did so for more such domains than did self-reports, suggesting that parental reports probably have greater validity. The higher rates of disorder they reported at outcome are probably the more accurate ones. Such adjustments for age and source of reporting, however, do not correct for the potentially increasing inappropriateness of the item sets for this aging sample, and so it is difficult to say how many of those not meeting these adjusted criteria may still have had the disorder.
A different issue pertains to whether or not the criteria should be adjusted for the gender of the children being diagnosed. Research evaluating these and similar item sets demonstrates that male youngsters display more of these items and to a more severe degree than do female youngsters in the general population (Achenbach, 1990; DuPaul et al., 1999). Given that the majority of children in the DSM field trial were boys (Lahey et al., 1994), the symptom threshold chosen in the DSM-IV is most appropriate to male children. This results in girls having to meet a higher threshold relative to other girls to be diagnosed as ADHD than do boys relative to other boys. Gender-adjusted thresholds for children would seem to be in order to address this problem, yet this would evaporate the currently disproportionate male-to-female ratio of 3:1 found across studies (see below). However, by adulthood, there appear to be no significant gender differences in ADHD symptoms Barkley, 2011a).
The requirement of an age of onset for ADHD symptoms (7-years-old) in the DSM-IV diagnostic criteria came under early attack from its own field trial (Applegate et al., 1997), a longitudinal study (McGee, Williams, & Feehan, 1992), and a review of this criterion from historical, empirical, and pragmatic perspectives (Barkley & Biederman, 1997). Although I have suggested that age 16 might serve as a better age of onset criterion for diagnosis because it captures more than 98% of all cases (Barkley et al., 2008), the DSM-5 has decided to raise the threshold to age 12-years-old. This serves to partially correct the problem in DSM-IV but may still leave 7%-10% of cases of ADHD ineligible for the diagnosis due to an age of onset later than this one.
A related potential problem for these criteria occurs in their failure to stipulate a lower bound age group for giving the diagnosis below which no diagnosis should be made. This is important because research on preschool children has shown that a separate dimension of hyperactive-impulsive behavior from aggression or defiant behavior does not seem to emerge until about 3-years-old (Achenbach & Edelbrock, 1987; Campbell, 1990). Below this age, these behaviors cluster together to form what has been called behavioral immaturity, externalizing problems, or an under-controlled pattern of conduct. This implies that the symptoms of ADHD may be difficult to distinguish from other early behavioral disorders until at least 3-years-old, and so this age might serve as a lower bound for diagnostic applications.
Similarly, research implies that a lower bound of IQ (IQ>50) might also be important, below which the nature of ADHD may be quite different. Minimal research seems to exist that speaks to the issue of a discontinuity or qualitative shift in the nature of ADHD in individuals below IQs of 50. Some indirect evidence implies that this may occur, however. Rutter and colleagues (Rutter, Bolton, et al., 1990; Rutter, Macdonald, et al., 1990) have concluded that children who fall below this level of IQ may have a qualitatively different form of mental retardation. This is inferred from findings that this group is over represented for its position along a normal distribution and from findings that genetic defects contribute more heavily to this subgroup. Given this shift in the prevalence and causes of mental retardation below this level of IQ, a similar state of affairs might exist for the form of ADHD associated with it necessitating its distinction from the type of ADHD that occurs in individuals above this IQ level. Consistent with such a view have been findings that the percentage of positive responders to stimulant medication falls off sharply below this threshold of IQ (Demb, 1991).
Another issue pertinent to the above is the problem of the duration requirement being set at six months. This has been chosen mainly out of tradition (earlier DSMs) with no research support for selecting this particular length of time for symptom presence. It is undoubtedly important that the symptoms be relatively persistent if we are to view this disorder as a developmental disability rather than arising purely from context or out of a transient, normal developmental stage. Yet specifying a precise duration is difficult in the absence of much research to guide the issue. Research on preschool-aged children might prove helpful here, however. Such research has shown that many children aged 3-years-old (or younger) may have parents or preschool teachers who report concerns about the activity level or attention of the children, yet these concerns have a high likelihood of remission within 12 months (Beitchman, Wekerle, & Hood, 1987; Campbell, 1990; Lerner, Inui, Trupin, & Douglas, 1985; Palfrey, Levine, Walker, & Sullivan, 1985). It would seem for preschoolers that the six month duration specified in the DSM-IV may be too brief, resulting in over-identification of ADHD children at this age (false positives). However, this same body of research found that for those children whose problems lasted at least 12 months or beyond age 4-years-old, the behavior problems were highly persistent and predictive of continuance into the school-age range. Such research suggests that the duration of symptoms be set at 12 months or more.
The DSM requirement that the symptoms be demonstrated in at least two of three environments so as to establish pervasiveness of symptoms is new to this edition and problematic. The DSM implies that two of three sources of information (parent, teacher, employer) must agree on the presence of the symptoms. This confounds settings with sources of information. The degree of agreement between parents and teacher for any dimension of child behavior is modest, often ranging between .30 and .50 (Achenbach, McConaughy, & Howell, 1987). This sets an upper limit on the extent to which parents and teachers are going to agree on the severity of ADHD symptoms and, thus, on whether or not the child has the disorder in that setting. Such disagreements among sources certainly reflect differences in the child’s behavior as a function of true differential demands of these settings. But they also reflect differences in the attitudes and judgments between different people. Insisting on such agreement may reduce the application of the diagnosis to some children unfairly as a result of such well-established differences between parent and teacher opinions. It may also create a confounding of the disorder with issues of comorbidity with oppositional defiant disorder (ODD) (Costello, Loeber, & Stouthamer-Loeber, 1991). Parent-only identified ADHD children may have predominantly ODD with relatively milder ADHD, whereas teacher-only identified ADHD children may have chiefly ADHD and minimal or no ODD symptoms. Children identified by both parents and teachers as ADHD may, therefore, carry a higher likelihood of ODD. They may also simply reflect a more severe condition of ADHD than do the home- or school-only cases, being different in degree rather than in kind. Research is clearly conflicting on the matter (Cohen & Minde, 1983; Rapoport, Donelly, Zametkin, & Carrougher, 1986; Schachar, Rutter, & Smith, 1981; Taylor, Sandberg, Thorley, & Giles, 1991). Considering that teacher information on children is not always obtainable or convenient, that parents can convey the essence of that information to clinicians, and that diagnosis based on parents’ reports will lead to a diagnosis based on teacher reports 90% of the time (Biederman, Keenan, & Faraone, 1990), one may infer that parent reports could suffice for diagnostic purposes for now. However, more recent evidence suggests that the best discrimination of ADHD children from other groups might be achieved by blending the reports of parents and teachers such that one counts the number of different symptoms endorsed across both sources of information (Crystal, Ostrander, Chen, & August, 2001; Mitsis, McKay, Schulz, Newcorn, & Halperin, 2000).
Social critics in prior decades (Breggin, 1999; Kohn, 1989; Schrag & Divoky, 1975) and the Church of Scientology via its Citizens Commission on Human Rights routinely have charged that professionals have been too quick to label energetic and exuberant children as having a mental disorder. They also assert that educators may be using these labels as an excuse for simply poor educational environments. In other words, children who are hyperactive or ADHD are actually normal but are being labeled as mentally disordered because of parent and teacher intolerance (Kohn, 1989) or lack of love at home (Breggin, 1999). If this were actually true, then we should find no differences of any cognitive, neurological, genetic, behavioral, or social significance between children so labeled and normal children. We should also find that the diagnosis of ADHD is not associated with any significant risks later in development for maladjustment within any domains of adaptive functioning, or social, occupational, or school performance. Furthermore, research on potential etiologies for the disorder should, likewise, come up empty-handed. This is hardly the case, as evidence reviewed in this chapter attests. Differences between ADHD and normal children are too numerous to take these assertions of normality seriously. As will be shown later, substantial developmental risks await the child meeting clinical diagnostic criteria for the disorder, and certain potential etiological factors are becoming consistently noted in the research literature.
Conceding all of this, however, does not automatically entitle ADHD to be placed within the realm of valid (“real”) disorders. Wakefield (1999) has argued that disorders must meet two criteria to be viewed as valid: (1) engender substantial harm to the individual or those around him or her and (2) incur dysfunction of natural and universal mechanisms that have been selected in an evolutionary sense (have survival value). The latter criterion is simply the definition of an adaptation as used in evolutionary biology. Disorders are failures in adaptations that produce harm. In the case of psychology, these universal mechanisms are psychological ones possessed by all normally developing humans, regardless of culture. ADHD handily meets both criteria (Barkley, 2006; Barkley et al., 2008). Those with ADHD, as described in the theory presented below, have significant deficits in behavioral inhibition and inattention (the executive functions) that are critical for effective self-regulation. And, those with ADHD experience numerous domains of impairment (risks of harm) over development, as will become evident below.
The prevalence of ADHD varies across studies, at least in part, due to different methods of selecting samples, the nature of the populations from which they are drawn (nationality or ethnicity, urban vs. rural, community vs. primary care settings, etc.), the criteria used to define ADHD (DSM criteria vs. rating scale cutoff), and certainly to the age range and sex composition of the samples. When only the endorsement of the presence of the behavior of hyperactivity (not the clinical disorder) is required from either parent or teacher rating scales, prevalence rates can run as high as 22% to 57% (Lapouse & Monk, 1958; McArdle, O’Brien, & Kolvin, 1995; Werry & Quay, 1971). This underscores the point made earlier that being described as inattentive or overactive by a parent or teacher does not in and of itself constitute a disorder in a child. When diagnostic criteria such as those in the DSM are used, prevalence rates are between 7% and 10% of children (Lingineni et al., 2012) and 2.5% to 5.5% of adults (Barkley, 2011a; Simon et al., 2012).
The most accurate assessments of prevalence come from two large-scale studies. One was a meta-analysis of worldwide prevalence studies that reported an average of 5.5% of children (Polanczyk et al., 2007) while an epidemiological study of U.S. adults as well as a worldwide prevalence study placed the prevalence at 3.4% to 4.4% (Fayyad et al., 2007; Kessler et al., 2006).
Prevalence varies as a function of young age, male gender, chronic health problems, family dysfunction, low socioeconomic status, presence of a developmental impairment, and urban living. (Lavigne et al., 1996; Velez, Johnson, & Cohen, 1989).
As noted above in discussing DSM criteria, it may be that the declining prevalence of ADHD with age is partly due to the types of items contained in the DSM symptom list that are chiefly applicable to young children. This could create a situation where individuals remain impaired in the construct(s) comprising ADHD, such as inhibition and executive functioning, as they mature, while outgrowing the symptom list for the disorder, resulting in an illusory decline in prevalence. This was noted in my Milwaukee follow-up study discussed above. Until more age-appropriate symptoms are studied for adolescent and adult populations, this issue remains unresolved.
As noted above, gender appears to play a significant role in determining prevalence of ADHD within the childhood population. On average, male children are between 2.5 and 5.6 times more likely than female children to be diagnosed as ADHD within epidemiological samples, with the average being roughly 3:1 (Polanczyk et al., 2007). This is not the case by adulthood (Barkley, 2011a; Fayyad et al., 2007; Kessler et al., 2006). Within clinic-referred samples, the gender ratio can be considerably higher, suggesting that boys with ADHD are far more likely to be referred to clinics than girls. This is probably because boys are more likely to have a comorbid oppositional or conduct disorder.
Studies of clinic-referred girls often find that they are as impaired as clinic-referred boys with ADHD, have as much comorbidity, and may even have greater deficits in intelligence, according to meta-analytic reviews of gender differences in ADHD (Gaub & Carlson, 1997; Gershon, 2001). Some studies suggest these clinic-referred girls, at least as adolescents, may have more internalizing symptoms, such as depression, anxiety, and stress, greater problems with teacher relationships, and poorer verbal abilities (vocabulary) in comparison to ADHD boys (Rucklidge & Tannock, 2001). Like the boys, girls with ADHD also manifest more conduct, mood, and anxiety disorders, have lower intelligence, and have greater academic achievement deficits than do control samples (Biederman, Faraone, et al., 1999; Rucklidge & Tannock, 2001). Males with ADHD may have greater problems with cognitive processing speed than females but these differences were no longer significant after controlling for severity of ADHD (Rucklidge & Tannock, 2001). No gender differences have been identified in executive functioning as measured by cognitive tests, with both genders being more impaired than control samples on such measures (Barkley, 2006; Barkley et al., 2008; Castellanos et al., 2000; Murphy et al., 2001). In contrast, studies drawing their ADHD samples from the community find that girls are significantly less likely to have comorbid ODD and CD than boys with ADHD, do not have greater intellectual deficits than ADHD boys, yet may be as socially and academically impaired as boys with the disorder (Gaub & Carlson, 1997; Gershon, 2001; Green et al., 2001).
Few studies have examined the relationship of ADHD to social class, and those that have are not especially consistent. Trites (1979), and later Szatmari (1992), both found that rates of ADHD tended to increase with lower socioeconomic class. However, in his own study Szatmari (Szatmari et al., 1989) found that low socioeconomic status was no longer associated with rates of ADHD when other comorbid conditions, such as conduct disorder, were controlled. For now, it is clear that ADHD occurs across all socioeconomic levels. Variations across social classes may be artifacts of the source used to define the disorder or of the comorbidity of ADHD with other disorders related to social class, such as oppositional defiant disorder and conduct disorder.
Early studies of the prevalence of hyperactivity, relying principally on teacher ratings, found significant disparities across four countries (United States, Germany, Canada, and New Zealand), ranging from 2% in girls and 9% in boys in the United States to 9% in girls and 22% in boys in New Zealand (Trites et al., 1979). Similarly, O’Leary, Vivian, and Nisi (1985) found rates of hyperactivity to be 3% in girls and 20% in boys in Italy using this same teacher rating scale and cutoff score. However, this may have resulted from the use of a threshold established on norms collected in the United States across these other countries, where the distributions were quite different from those found in the United States.
Later studies, especially those using DSM criteria, have found the disorder across all countries studied to date (Fayyad et al., 2007; Polanczyk et al., 2007).
Early studies found differences among ethnic groups in rates of hyperactivity within the United States. Langsdorf, Anderson, Walchter, Madrigal, and Juarez (1979) reported that almost 25% of African-American children and 8% of Latino-Americans met a cutoff score on a teacher rating scale commonly used to define hyperactivity, whereas Ullmann (cited in O’Leary et al., 1985) reported rates of 24% for African-American children and 16% of white Americans on a teacher rating scale. Such differences, however, may arise in part because of socioeconomic factors that are differentially associated with these ethnic groups in the United States. Such psychosocial factors are strongly correlated with aggression and conduct problems. As noted above, those factors no longer make a significant contribution to the prevalence of ADHD when comorbidity for other disorders is controlled (Szatmari, 1992). Doing the same within studies of ethnic differences might well reduce or eliminate these differences in prevalence among them. In a recent survey of U.S. adults, Barkley (2011a) found no significant differences among ethnic groups except a slightly higher level of hyperactivity reported in Hispanic-Latino males. Thus, it would seem that ADHD exists in all ethnic groups studied so far. Whether the differences in prevalence across these ethnic groups are real or are a function of the source of information about the symptoms of ADHD and, possibly, socioeconomic factors remains to be determined.
Major follow-up studies of clinically referred hyperactive children have been ongoing during the last 25 years at five sites: (1) Montreal (Weiss & Hechtman, in press), (2) New York City (Gittelman, Mannuzza, Shenker, & Bonagura, 1985; Klein et al., 2012; Mannuzza, Gittelman-Klein, Bessler, Malloy, & Lapadulo, 1993), (3) Iowa City (Loney, Kramer, & Milich, 1981), (4) Los Angeles (Satterfield, Hoppe, & Schell, 1982), and (5) Milwaukee (Barkley, Fischer, et al., 1990; Barkley, Fischer et al., 2002; Barkley et al., 2008). Follow-up studies of children identified as hyperactive from a general population have also been conducted in the United States (Lambert, 1988), New Zealand (McGee, Williams, & Silva, 1984; Moffitt, 1990), and England (Taylor et al., 1991), among others.
But before embarking on a summary of their results, some cautionary notes are in order.The differing entry/diagnostic criteria across follow-up studies must be kept in mind in interpreting and cross-referencing their outcomes. Most studies selected for children known at the time as “hyperactive.” Such children are most likely representative of the course of the ADHD Combined Type from the current DSM taxonomy. Even then, the degree of deviance of the samples on parent and teacher ratings of these symptoms was not established at the entry point in most of these studies. These studies also cannot be viewed as representing the Inattentive subtype from DSM-IV or now the new SCT group of children and adults, for which no follow-up information is currently available. The descriptions of clinic-referred ADHD children who are of similar age groups to those in the follow-up studies but who are not followed over time may help understand the risks associated with different points in development. However, these may also be contaminated by cohort effects at the time of referral and so can only be viewed as suggestive. Such cohort effects may be minor; that is, adolescents with ADHD referred to clinics seem to have similar types and degrees of impairment as ADHD children followed up to adolescence (Barkley, Anastopoulos, Guevremont, & Fletcher, 1991 vs. Barkley, Fischer, et al., 1990).
The average onset of ADHD symptoms, as noted earlier, is often in the preschool years, typically at ages 3 to 4-years-old (Applegate et al., 1997; Loeber et al., 1992; Taylor et al., 1991) and, more generally, by entry into formal schooling. Yet, as noted earlier, only half of all ADHD cases have developed by age 7-years-old while 93% have developed by age 12-years-old and >98% by age 16-years-old (Barkley et al., 2008).
Preschool-aged children who are perceived as difficult and resistant to control or who have inattentive and hyperactive behavior that persists for at least a year or more are highly likely to have ADHD and to remain so into elementary school years (Beitchman et al., 1987; Campbell, 1990; Palfrey et al., 1985) and even adolescence (Olson, Bates, Sandy, & Lanthier, 2000). Persistent cases seem especially likely to occur where parent-child conflict, greater maternal directiveness and negativity, and greater child defiant behavior exist (Campbell, March, Pierce, & Ewing, 1991; Olson et al., 2000; Richman, Stevenson, & Graham, 1982). More negative temperament and greater emotional reactivity to events are also more common in preschool ADHD children (Barkley, DuPaul, & McMurray, 1990; Campbell, 1990). It is little wonder that greater parenting stress is associated with preschool ADHD children and seems to be at its highest relative to later age groups (Mash & Johnston, 1983a, 1983b). Within the preschool setting, ADHD children will be found to be more often out of their seats, wandering the classroom, being excessively talkative and vocally noisy, and disruptive of other children’s activities (Campbell, Schleifer, & Weiss, 1978; Schleifer et al., 1975).
By the time ADHD children move into the elementary-age range of 6 to 12-years-old, the problems with hyperactive-impulsive behavior are likely to continue and to be joined now by difficulties with attention (executive functioning and goal-directed persistence. Difficulties with work completion and productivity, distraction, forgetfulness related to what needs doing, lack of planning, poor organization of work activities, trouble meeting time deadlines associated with home chores, school assignments, and social promises or commitments to peers are now combined with the impulsive, heedless, and disinhibited behavior typifying these children since preschool age. Problems with oppositional and socially aggressive behavior may emerge at this age in at least 40% to 70% of ADHD children (Barkley, 2006; Loeber et al., 1992; Taylor et al., 1991).
By ages 8 to 12-years-old, these early forms of defiant and hostile behavior may evolve further into symptoms of conduct disorder in 25% to 45% or more of all children with ADHD (Barkley, Fischer, et al., 1990; Gittelman et al., 1985; Loeber et al., 1992; Mannuzza et al., 1993; Taylor et al., 1991). Certainly by late childhood most or all of the deficits in the executive functions are likely to be arising and interfering with adequate self-regulation (Barkley, 1997b). Not surprisingly, the overall adaptive functioning (self-sufficiency) of many ADHD children (Stein, Szumowski, Blondis, & Roizen, 1995) is significantly below their intellectual ability. This is also true of preschoolers with high levels of these externalizing symptoms (Barkley et al., 1998). The disparity between adaptive functioning and age appropriate expectations (or IQ) may itself be a predictor of greater severity of ADHD as well as risk for oppositional and conduct problems in later childhood (Barkley, Shelton, et al., 2002). The disorder takes its toll on self-care, personal responsibility, chore performance, trustworthiness, independence, appropriate social skills, and timeliness, specifically, and moral conduct generally (Barkley, 2006; Hinshaw et al., 1993).
If ADHD is present in clinic-referred children, the likelihood is that 50% to 80% will continue to have their disorder into adolescence, with most studies supporting the higher figure (August, Stewart & Holmes, 1983; Claude & Firestone, 1995; Barkley, Fischer, et al., 1990; Gittelman et al., 1985; Mannuzza et al., 1993). Using the same parent rating scales at both the childhood and adolescent evaluation points, Fischer et al. (1993a) were able to show that inattention, hyperactive-impulsive behavior, and home conflicts declined by adolescence. The hyperactive group showed far more marked declines than the control group, mainly because the former were so far from the mean of the normative group to begin with in childhood. Nevertheless, even at adolescence, the groups remained significantly different in each domain with the mean for the hyperactives remaining two standard deviations or more above the mean for the controls. This emphasizes the point made earlier that simply because severity levels of symptoms are declining over development does not mean hyperactive children are necessarily outgrowing their disorder relative to normal children. Like mental retardation, ADHD may need to be defined by a developmentally relative deficiency, rather than an absolute one, that persists in most children over time.
The persistence of ADHD symptoms across childhood as well as into early adolescence appears, again, to be associated with the initial degree of hyperactive-impulsive behavior in childhood, the coexistence of conduct problems or oppositional hostile behavior, poor family relations and specifically conflict in parent-child interactions, as well as maternal depression, and duration of mental health interventions (Fischer et al., 1993b; Taylor et al., 1991). These predictors have also been associated with the development and persistence of oppositional and conduct disorder into this age range (12 to 17-years-old; Barkley, 2013; Fischer et al., 1993b; Loeber, 1990; Mannuzza & Klein, 1992; Taylor et al., 1991).
Studies following large samples of clinic-referred children with hyperactivity (or ADHD) into adulthood are few in number. Only four follow-up studies have retained at least 50% or more of their original sample into adulthood and reported on the persistence of symptoms to that time. These are the Montreal study by Weiss, Hechtman, and their colleagues (see Weiss & Hechtman, 1993), the New York City study by Mannuzza, Klein, and colleagues (see Klein et al., 2012; Mannuzza, Klein, Bessler, Malloy, & LaPadula, 1993, 1998), the Swedish study by Rasmussen and Gillberg (2001), and my research with Mariellen Fischer in Milwaukee (Barkley et al., 2008; Barkley, Fischer et al., 2002; Fischer et al., 2002). The results regarding the persistence of disorder into young adulthood (middle 20s) are mixed but can be better understood as being a function of reporting source and the diagnostic criteria used (Barkley et al., 2002).
The Montreal study (N=103) found that two-thirds of their original sample (N=64; mean age of 25 years) claimed to be troubled as adults by at least one or more disabling core symptoms of their original disorder (restlessness, impulsivity, or inattention) and that 34% had at least moderate to severe levels of hyperactive, impulsive, and inattentive symptoms (Weiss & Hechtman, 1993, p. 73). In Sweden (N=50), Rasmussen and Gillberg (2001) obtained similar results, with 49% of probands reporting marked symptoms of ADHD at age 22 years compared to 9% of controls. Formal diagnostic criteria for ADHD, as in DSM-III or later editions, were not employed at any of the outcome points in either study, however. In contrast, the New York study has followed two separate cohorts of hyperactive children using DSM criteria to assess persistence of disorder. That study found that 31% of their initial cohort (N=101) and 43% of their second cohort (N=94) met DSM-III criteria for ADHD by ages 16-23 (mean age=18.5 years) (Gittelman, et al. 1985; Mannuzza et al., 1991). Eight years later, (mean age 26 years), however, these figures fell to 8% and 4%, respectively (now using DSM-III-R criteria) (Mannuzza et al., 1993, 1998). At 30-year follow-up, the rate of ADHD diagnosed using DSM-IV criteria and by self-report was 22%. Those results might imply that the vast majority of hyperactive children no longer qualify for the diagnosis of ADHD by adulthood.
The interpretation of the relatively low rate of persistence of ADHD into adulthood, particularly for the New York study, is clouded by at least two issues apart from differences in selection criteria. One is that the source of information about the disorder changed in all of these studies from that used at the childhood and adolescent evaluations to that used at the adult outcome. At study entry and at adolescence, all studies used the reports of others (parents and typically teachers). By mid-adolescence, all found that the majority of hyperactive participants (50% to 80%) continued to manifest significant levels of the disorder (see above). In young adulthood (approximately age 26-years-old), both the New York and Montreal studies switched to self-reports of disorder.
The rather marked decline in persistence of ADHD from adolescence to adulthood could stem from this change in source of information. Indeed, the New York study found this to be likely when, at late adolescence (mean age of 18 to 19-years-old), they interviewed both the teenagers and their parents about psychiatric status of the teens (Mannuzza & Gittelman, 1986). There was a marked disparity between the reports of parents and teens concerning the presence of ADHD (11% vs. 27%; agreement 74%, Kappa=.19). Other research also suggests that the relationship between older children’s (age 11-years-old) self-reports of externalizing symptoms, such as those involved in ADHD, and those of parents and teachers is quite low (r=.16-.32; Henry, Moffitt, Caspi, Langley, & Silva, 1994). Thus, changing sources of reporting in longitudinal studies on behavioral disorders could be expected to lead to marked differences in estimates of persistence of those disorders.
The question obviously arises as to whose assessment of the proband is more accurate. This would depend on the purpose of the assessment, but the prediction of impairment in major life activities would seem to be an important one in research on psychiatric disorders. Our Milwaukee study examined these issues by interviewing both the participants and their parents about ADHD symptoms at the young adult follow-up (age 21-years-old). It then examined the relationship of each source’s reports to significant outcomes in major life activities (education, occupation, social, etc.) after controlling for the contribution made by the other source. As noted earlier, another limitation in the earlier studies may reside in the DSM criteria in that they grow less sensitive to the disorder with age. Using a developmentally referenced criterion (age comparison) to determine diagnosis may identify more cases than would the DSM approach. As discussed earlier, the Milwaukee study found that the persistence of ADHD into adulthood was heavily dependent on the source of the information (self or parent) and the diagnostic criteria (DSM or developmentally referenced). Self-report identified just 5% to 12% of probands as currently ADHD (DSM-III-R) while parent reports placed this figure at 46% to 66%. Using the DSM resulted in lower rates of persistence (5% for proband reports and 46% for parents) while using a developmentally referenced cutoff (98th percentile) yielded higher rates of persistence (12% by self-report and 66% by parent reports). Parental reports appeared to have greater validity in view of their greater contribution to impairment and to more domains of current impairment than did self-reported information (Barkley et al., 2002; Barkley et al., 2008). We concluded that past follow-up studies grossly under-estimated the persistence of ADHD into adulthood by relying solely on the self-reports of the probands and using DSM criteria at adulthood; criteria developed only for children. As discussed above, using a childhood threshold for symptoms, such as six, with adults may be inappropriate whereas a lower threshold of four symptoms may be more accurate in detecting the disorder in older age groups. For instance, at a age 27 follow-up, persistence of disorder was estimated to be 65% to 86% depending on the rigor of the definition of recovery (Barkley et al., 2008)
Individuals diagnosed with ADHD are often found to have a number of other disorders besides their ADHD (Barkley, 2006; Brown, 2011). What is known about comorbidity is largely confined to the Combined Type of ADHD. In community derived samples, up to 44% of ADHD children have at least one other disorder and 43% have at least two or more additional disorders (Szatmari et al., 1989a). The figure is higher, of course, for children drawn from clinics. As many as 87 percent of clinically diagnosed ADHD children may have at least one other disorder and 67% have at least two other disorders (Kadesjo & Gillberg, 2001). Results for adults with ADHD are nearly as high, with more than 80% having at least one disorder and more than 50% having two or more (Barkley et al., 2008). The disorders likely to co-occur with ADHD are briefly described below.
The most common comorbid disorders with ADHD are oppositional defiant disorder (ODD) and, to a lesser extent, conduct disorder (CD). Indeed, the presence of ADHD increases the odds of ODD/CD by 10.7 fold (95% Confidence Interval [CI] = 7.7-14.8) in general population studies (Angold, Costello, & Erkanli, 1999). Studies of clinic-referred ADHD children find that between 54% and 67% will meet criteria for a diagnosis of ODD by 7-years-old or later. ODD is a frequent precursor to CD, a more severe and often (though not always) later occurring stage of ODD (Loeber, Burke, Lahey, Winters, & Zera, 2000). The co-occurrence of CD with ADHD may be 20% to 50% in children and 44% to 50% in adolescence with ADHD (Barkley, 2006; Barkley et al., 1990; Biederman et al., 1992; Lahey, McBurnett, & Loeber, 2000; Waschbusch, 2002). By adulthood, up to 26% may continue to have CD while 12% to 21% will qualify for antisocial personality disorder (ASPD) (Biederman et al., 1992; Barkley, Fischer, Smallish, & Fletcher, 2002; Mannuzza & Klein, 1992; Rasmussen & Gillberg, 2001; Weiss & Hechtman, 1993). Similar or only slightly lower degrees of overlap are noted in studies using epidemiologically identified samples rather than those referred to clinics. ADHD, therefore, has a strong association with conduct problems and antisocial disorders, such as ODD, CD, and ASPD, and has been found to be one of the most reliable early predictors of these disorders (Fischer et al., 1993b; Hinshaw & Lee, 2002; Lahey et al., 2000). Recent longitudinal research suggests that severity of early ADHD is actually a contributing factor to risk for later ODD regardless of severity of early ODD (Burns & Walsh, 2001), perhaps due to the problems with poor emotion (anger) regulation in ADHD noted above (Barkley, 2010). Familial associations among the disorders have also been consistently found, whether across boys and girls with ADHD or across Caucasian and African-American samples (Biederman et al., 1992; Faraone, Biederman, Mick, et al., 2000; Samuel et al., 1999). This suggests some underlying causal connection among these disorders. Evidence from twin studies indicates a shared or common genetic contribution to the three disorders, particularly between ADHD and ODD (Coolidge, Thede, & Young, 2000; Silberg et al., 1996). When CD occurs in conjunction with ADHD, it may represent simply a more severe form of ADHD having a greater family genetic loading for ADHD (Thapar, Harrington, & McGuffin, 2001). Other research, however, also suggests a shared environmental risk factor may also account for the overlap of ODD and CD with ADHD beyond their shared genetics (Burt, Krueger, McGue, & Iacono, 2001), that risk factor likely being family adversity generally and impaired parenting specifically (Patterson, Degarmo, & Knutson, 2000). To summarize, ODD and CD have a substantial likelihood of co-occurring with ADHD with the risk for ODD/CD being mediated in large part by severity of ADHD and its family genetic loading and in part by adversity in the familial environment.
One of the strongest predictors of risk for substance use and abuse disorders (SUDs) among ADHD children upon reaching adolescence and adulthood is prior or co-existing CD or ASPD (Barkley et al., 2008; Burke, Loeber, & Lahey, 2001; Chilcoat & Breslau, 1999; Molina & Pelham, 1999)). Given the heightened risk for ODD/CD/ASPD in ADHD children as they mature, one would naturally expect a greater risk for SUDs as well. Yet, ADHD alone is a predictor of adolescent and adult alcohol and nicotine use (Barkley et al., 2008; Charach et al., 2012) and probably some illicit drug use (Gudjonsson et al., 2012).
The overlap of anxiety disorders with ADHD has been found to be 10% to 40% in clinic-referred children, averaging to about 25% (see Barkley, 2006; Biederman, Newcorn, & Sprich, 1991; Schatz & Rostain, 2006; Tannock, 2011, for reviews). In longitudinal studies of ADHD children, however, the risk of anxiety disorders is no greater than in control groups at either adolescence or young adulthood (Mannuzza et al., 1993, 1998; Russo & Biedel, 1994; Weiss & Hechtman, 1993) but does rise to 33% of those children whose ADHD persists to age 27 (Barkley et al., 2008). The disparity in findings for children is puzzling. Perhaps some of the overlap of ADHD with anxiety disorders in children is due to referral bias (Biederman, Faraone, & Lapey, 1992; Tannock, 2011). General population studies of children, however, do suggest an elevated odds ratio of having an anxiety disorder in the presence of ADHD of 3.0 (95%CI = 2.1-4.3), with this relationship being significant even after controlling for comorbid ODD/CD (Angold et al., 1999). This implies that the two disorders may have some association apart from referral bias, at least in childhood. The co-occurrence of anxiety disorders with ADHD has been shown to reduce the degree of impulsiveness relative to those ADHD children without anxiety disorders (Pliszka, 1992; Schatz & Rostain, 2006). Some research suggests that the disorders are transmitted independently in families and so are not linked to each other in any genetic way (Biederman et al., 1991; Last, Hersen, Kazdin, Orvaschel, & Perrin, 1991). This may not be the case for the DSM-IV inattentive type of ADHD or what is now called SCT, where higher rates of anxiety disorders have been noted in some studies of these children (see Milich et al., 2001 for a review; Russo & Biedel, 1994; Schatz & Rostain, 2006), though not always (Barkley, 2012b; Barkley, DuPaul, & McMurray, 1990), and in their first- and second-degree relatives (Barkley, DuPaul, & McMurray, 1990; Biederman et al., 1992) again though not always (Lahey & Carlson, 1992; Milich et al., 2001). Regrettably, research on the overlap of anxiety disorders with ADHD has generally chosen to collapse across the types of anxiety disorders in evaluating this issue. Greater clarity and clinical utility from these findings might occur if the types of anxiety disorders present were to be examined separately.
The evidence for the co-occurrence of mood disorders, such as major depression or dysthymia (a milder form of depression), with ADHD is now fairly substantial (Daviss, 2008; Faraone & Biederman, 1997; Jensen, Martin, & Cantwell, 1997; Spencer, Wilens, Biederman, Wozniak & Crawford, 2000 for reviews). Between 15% and 75% of those with ADHD may have a mood disorder, though most studies place the association between 20% and 30% (Barkley, 2006; Barkley et al., 2008; Biederman et al., 1992; Cuffe et al, 2001; Fischer et al., 2002). The odds of having depression given the presence of ADHD in general population samples is 5.5 (95% CI 3.5-8.4) (Angold et al., 1999). Some evidence also suggests that these disorders may be related to each other in that familial risk for one disorder substantially increases the risk for the other (Biederman et al., 1991, 1992; Faraone & Biederman, 1997), particularly where ADHD is comorbid with CD. Similarly, a recent follow-up study (Fischer et al., 2002) found a 26% risk of major depression among ADHD children by young adulthood, but this risk was largely mediated by the co-occurrence of CD. Current depression fell to 14% of the ADHD cases by adulthood (Barkley et al., 2008). Likewise, a meta-analysis of general population studies indicated that the link between ADHD and depression was entirely mediated by the linkage of both disorders to CD (Angold et al., 1999). In the absence of CD, ADHD was not more likely to be associated with depression.
The comorbidity of ADHD with bipolar (manic-depressive) disorder is controversial (Carlson, 1990; Geller & Luby, 1997). Some studies of ADHD children indicate that 10% to 20% may have bipolar disorder (Milberger, Biederman, Faraone, Murphy, & Tsuang, 1995; Spencer et al., 2000; Wozniak et al., 1995) – a figure substantially higher than the 2% risk for the general population (Lewinsohn, Klein, & Seeley, 1995; Skirrow et al., 2012; Youngstrom, 2010). Follow-up studies of hyperactive children, however, have not documented any significant increase in risk of bipolar disorder in children with ADHD followed into adulthood with rates typically close to those for the general population (Fischer et al., 2002; Klein et al., 2012; Mannuzza et al., 1993, 1998; Weiss & Hechtman, 1993). However, that risk would have to exceed 7% or more for these studies to have sufficient power to detect any comorbidity. A four-year follow-up of ADHD children reported that 12% met criteria for bipolar disorder in adolescence (Biederman, Faraone, Mick, Wozniak et al., 1996). ADHD children without bipolar disorder do not have an increased prevalence of bipolar disorder among their biological relatives (Biederman et al., 1992; Faraone, Biederman, & Monuteaux, 2001; Lahey et al., 1988), while ADHD children with bipolar disorder do (Faraone, Biederman, Wozniak, Mundy, Mennin, & O’Donnell, 1997; Faraone et al., 2001), suggesting that where the overlap occurs it may represent a familially distinct subset of ADHD. Children and adolescents diagnosed with childhood bipolar disorder often have a significantly higher lifetime prevalence of ADHD, particularly in their earlier childhood years (Carlson, 1990; Geller & Luby, 1997; Strober et al., 1988). Where the two disorders co-exist, the onset of bipolar disorder may be earlier than in bipolar disorder alone (Faraone et al., 1997; Faraone et al., 2001; Sachs, Baldassano, Truman, & Guille, 2000). In bipolar cases that start in adulthood, comorbidity with ADHD may be only 20% to 25% while it may average 62% and in some studies be as high as 80% to 97% in cases where bipolar disorder begins in childhood (Skirrow et al., 2012; Youngstrom, 2010). Some of this overlap with ADHD may be partly an artifact of similar symptoms comprising the symptom lists used for both diagnoses (i.e., hyperactivity, distractibility, poor judgment, etc.) (Geller & Luby, 1997; Skirrow et al., 2012; Youngstrom, 2010). In any case, the overlap of ADHD with bipolar disorder appears to be unidirectional – a diagnosis of ADHD seems not to increase the risk for bipolar disorder, whereas a diagnosis of childhood bipolar disorder seems to dramatically elevate the risk of a prior or concurrent diagnosis of ADHD (Geller & Luby, 1997; Spencer et al., 2000; Skirrow et al., 2012).
Up to 18% of children may develop a motor tic in childhood that declines to a base rate of about 2% by mid-adolescence and less than 1% by adulthood (Peterson, Pine, Cohen, & Brook, 2001). The risk for tics among children with ADHD is only slightly higher than this; about 20% (Simpson et al., 2011). Tourette’s Disorder (TD), a more severe disorder involving multiple motor and vocal tics, occurs in less than 0.4% of the population (Peterson et al., 2001). A diagnosis of ADHD does not appear to necessarily elevate these risks for a diagnosis of tics or Tourette’s Disorder, at least not in childhood or adolescence (Peterson et al., 2001). Among clinic-referred adults diagnosed with ADHD, there may be a slightly greater occurrence of tic disorders (12%; Spencer et al., 2001). In contrast, individuals with obsessive-compulsive disorder (OCD) or TD have a marked elevation in risk for ADHD, averaging 48% or more (range 35% to 71%; Comings, 2000; Simpson et al., 2011). Complicating matters is the fact that the onset of ADHD often seems to precede that of TD in cases of comorbidity (Comings, 2000).
Apart from an increased risk for various psychiatric disorders, children and teens with ADHD are also more likely to experience a substantial array of developmental and health risks, discussed below. Far less is known about the extent to which these correlated problems are evident in the Inattentive Type, particularly the subgroup having problems with sluggish cognitive tempo described above. The developmental and social problems most likely to occur with ADHD are briefly listed in Table 1.2. (From Barkley, 2006).
Table 1.2: Summary of Impairments Likely to be Associated with ADHD
As a group, as many as 60% of ADHD, compared to up to 35% of normal children, may have poor motor coordination or developmental coordination disorder (Barkley, DuPaul, & McMurray, 1990; Hartsough & Lambert, 1985; Kadesjo & Gillberg, 1999; Szatmari et al., 1989b; Stewart et al., 1966). Neurological examinations for "soft" signs related to motor coordination and motor overflow movements find ADHD children to demonstrate more such signs as well as generally sluggish gross motor movements than control children, including those with purely learning disabilities (Carte, Nigg, & Hinshaw, 1996; Denckla & Rudel, 1978; Denckla, Rudel, Chapman, & Krieger, 1985; McMahon & Greenberg, 1977; Shaywitz & Shaywitz, 1985; Werry et al., 1972). These overflow movements have been interpreted as indicators of delayed development of motor inhibition (Denckla et al., 1985).
Studies using tests of fine motor coordination, such as balance, fine motor gestures, electronic or paper-and-pencil mazes, and pursuit tracking often find children with ADHD to be less coordinated in these actions (Hoy et al., 1978; Mariani & Barkley, 1997; McMahon & Greenberg, 1977; Moffitt, 1990; Shaywitz & Shaywitz, 1985; Ullman et al., 1978). Simple motor speed, as measured by finger-tapping rate or grooved pegboard tests, does not seem to be as affected in ADHD as is the execution of complex, coordinated sequences of motor movements (Barkley, Murphy, & Kwasnik, 1996a; Breen, 1989; Grodzinsky & Diamond, 1992; Mariani & Barkley, 1997; Marcotte & Stern, 1997; Seidman et al., 1995, 1996). The vast majority of the available research, therefore, supports the existence of deficits in motor control, particularly when motor sequences must be performed, in those with ADHD.
The vast majority of clinic-referred children with ADHD have difficulties with school performance, most often under-productivity of their work. ADHD children frequently fall below normal or control groups of children on standardized achievement tests (Barkley, 2006; Barkley, DuPaul, & McMurray, 1990; Fischer et al., 1990; Hinshaw, 1992, 1994; Langberg et al., 2011; Loe & Feldman, 2007). Difficulties with academic performance are predicted more by inattention than HI symptoms while disruptive behavior is related more to the latter than the former. These differences from typically developing children are likely to be found even in preschool-age children with ADHD (Barkley, Shelton, et al., 1998; Mariani & Barkley, 1997), suggesting that the disorder may take a toll on the acquisition of academic skills and knowledge even before entry into first grade. This makes sense given that inattention symptoms are highly correlated with executive functions believed to be disrupted by ADHD and that such executive functions are also likely to be involved in some forms of academic achievement (i.e., working memory in mental arithmetic or spelling; internalized speech in reading comprehension; verbal fluency in oral narratives and written reports, etc.).
Between 19% and 26% of children with ADHD are likely to have any single type of learning disability, conservatively defined as a significant delay in reading, arithmetic, or spelling relative to intelligence and achievement in one of these three areas at or below the 7th percentile (Barkley, 2006) with over 45% having at least one or more LDs (DuPaul, Gormley & Laracy, 2012). If the criterion of simply two grades below grade level is used, then as many as 80% of ADHD children in late childhood (age 11 years) may have learning disorders (Cantwell & Baker, 1992). Studies suggest that the risk for reading disorders among ADHD children is 16% to 39%, while that for spelling disorders is 24% to 27%, and for math disorders, the risk is 13% to 33% (August & Garfinkel, 1990; Barkley, 1990; Casey et al., 1996; DuPaul et al., 2012; Frick et al., 1991; Semrud-Clikeman et al., 1992).
While the finding that children with ADHD are more likely to have learning disabilities (Gross-Tsur, Shalev, & Amir, 1991; Tannock & Brown, 2000) might imply a possible genetic link between the two disorders, more recent research (Doyle, Faraone, Dure, & Biederman, 2001; Faraone et al., 1993; Gilger, Pennington, & DeFries, 1992) shows that the two sets of disorders are transmitted independently in families. Some subtypes of reading disorders associated with ADHD may share a common genetic etiology (Gilger et al., 1992). This may arise from the finding that early ADHD may predispose children toward certain types of reading problems, whereas early reading problems are not as likely to give rise to later symptoms of ADHD, though the two disorders may interact to reciprocally increase risk for the other over time (Chadwick, Taylor, Taylor, Heptinstall, & Danckaerts, 1999; Rabiner, Coie, & The Conduct Problems Research Group, 2000; Velting & Whitehurst, 1997; Wood & Felton, 1994). The picture is less clear for spelling disorders, where a common or shared genetic etiology to both ADHD and spelling disorder has been shown in a joint analysis of twin samples from London and Colorado (Stevenson, Pennington, Gilger, DeFries, & Gillis, 1993). This may result from the fact that early spelling ability seems to be linked to the integrity of working memory (Mariani & Barkley, 1997; Levy & Hobbes, 1989) that may be impaired in those with ADHD . Writing disorders have not received as much attention in research on ADHD, though handwriting deficits are often found among children with ADHD, particularly those having the Combined type of the disorder (Marcotte & Stern, 1997).
Rapport, Scanlan, and Denney (1999) provide some evidence for a dual pathway model of the link between ADHD and academic underachievement. Briefly, ADHD may predispose to academic underachievement through its contribution to a greater risk for ODD/CD and conduct problems in the classroom more generally, the net effect of which is to adversely impact productivity and general school performance. But ADHD is also associated with cognitive deficits not only in attention, but general intelligence (see below) and working memory (see above) all of which may have a direct and adverse impact on academic achievement. Supportive of this view as well are findings that it is more the inattention dimension of ADHD that is most closely associated with academic achievement problems than the hyperactive-impulsive dimension (Faraone, Biederman, Weber, 1998; Hynd et al. 1991; Marshall, Hynd, Handwaerck, et al., 1997). According to this dual pathway model, both pathways will require interventions if the marked association of ADHD with school under-achievement is to be addressed.
A higher prevalence of speech and language disorders has also been documented in many studies of ADHD children, typically ranging from 30% to 64% of the samples (Bellani et al., 2011; Gross-Tsur et al., 1991; Hartsough & Lambert, 1985; Humphries, Koltun, Malone, & Roberts, 1994; Szatmari et al., 1989; Taylor et al., 1991). The converse is also true; children with speech and language disorders have a higher than expected prevalence of ADHD (approximately 30% to 58%), among other psychiatric disorders (see Bellani et al., 2011; Tannock & Brown, 2011; Tannock & Schachar, 1996, for reviews on comorbidity with ADHD).
Clinic-referred ADHD children often have lower intelligence than control groups used in these same studies, particularly in verbal intelligence (Barkley, Karlsson, & Pollard, 1985; Mariani & Barkley, 1997; McGee et al., 1992; Moffitt, 1990; Stewart, Pitts, Craig, & Dieruf, 1966; Werry et al., 1987; Tillman et al., 2009). Differences in IQ have also been found between hyperactive boys and their normal siblings (Halperin & Gittelman, 1982; Tarver-Behring, Barkley, & Karlsson, 1985; Welner, Welner, Stewart, Palkes, & Wish, 1977). The differences found in these studies often range from 7 to 10 standard score points. Studies using both community samples (Hinshaw, Morrison, Carte, & Cornsweet, 1987; McGee, Williams, & Silva, 1984; Peterson et al., 2001) and behavior-problem samples (Sonuga-Barke, Lamparelli, Stevenson, Thompson, & Henry, 1994) also have found significant negative associations between degree of ADHD and intelligence (rs = -.25-.35). In contrast, associations between ratings of conduct problems and intelligence in children are often much smaller or even nonsignificant, particularly when hyperactive-impulsive behavior is partialed out of the relationship (Hinshaw et al., 1987; Lynam, Moffitt, & Stouthamer-Loeber, 1993; Sonuga-Barke et al., 1994). This implies that the relationship between IQ and ADHD is not likely to be a function of comorbid conduct problems (see Hinshaw, 1992, for a review). Much of the difference between ADHD and typically developing groups appears to be the result of EF deficits associated with ADHD (Tillman et al., 2009).
The interpersonal behaviors of those with ADHD, as noted earlier, are often characterized as more impulsive, intrusive, excessive, disorganized, engaging, aggressive, intense, and emotional. And so they are “disruptive” of the smoothness of the ongoing stream of social interactions, reciprocity, and cooperation that is an increasingly important part the children’s daily life with others (Barkley, 2010; Whalen & Henker, 1992).
Research finds that ADHD affects the interactions of children with their parents and, hence, the manner in which parents may respond to these children (Johnston & Mash, 2001). Those with ADHD are more talkative, negative and defiant, less compliant and cooperative, more demanding of assistance from others, and less able to play and work independently of their mothers (Barkley, 1985; Danforth et al., 1991; Gomez & Sanson, 1994; Johnston, 1997; Johnston & Mash, 2001). Their mothers are less responsive to the questions of their children, more negative and directive, and less rewarding of their children’s behavior (Danforth et al., 1991; Johnston & Mash, 2001). Mothers of ADHD children have been shown to give both more commands as well as more rewards to their ADHD sons than daughters (Barkley, 1989b; Befera & Barkley, 1984) but also to be more emotional and acrimonious in their interactions with their sons (Buhrmester, Camparo, Christensen, Gonzalez, & Hinshaw, 1992; Taylor et al., 1991). ADHD children and teens seem to be nearly as problematic for their fathers as their mothers (Buhrmester et al., 1992; Edwards et al., 2001; Johnston, 1997; Tallmadge & Barkley, 1983). Contrary to what may be seen in normal mother-child interactions, the mother-child conflicts in ADHD children and teens may actually increase when fathers join the interaction, especially in hyperactive boys (Buhrmester et al., 1992; Edwards et al., 2001). Such increased maternal negativity and acrimony toward sons in these interactions has been shown to predict greater noncompliance in classroom and play settings and greater covert stealing away from home, even when the level of the child’s own negativity and parental psychopathology are statistically controlled in the analyses (Anderson, Hinshaw, & Simmel, 1994). The negative parent-child interaction patterns also occur in the preschool age group (Cohen, Sullivan, Minde, Novak, & Keens, 1983; DuPaul, McGoey, Eckert, & VanBrakle, 2001) and may be even more negative and stressful (to the parent) in this age range (Mash & Johnston, 1982, 1990) than in later age groups. With increasing age, the degree of conflict in these interactions lessens but remains deviant from normal into later childhood (Barkley, Karlsson, & Pollard, 1985; Mash & Johnston, 1982) and adolescence (Barkley, Anastopoulos, Guevremont, & Fletcher, 1992; Barkley, Fischer, et al., 1991; Edwards et al., 2001). Negative parent-ADHD child interactions in childhood have been observed to be significantly predictive of continuing parent-teen conflicts eight to 10 years later in adolescence in families with ADHD children (Barkley, Fischer, et al., 1991). Few differences are noted between the interactions of mothers of ADHD children with those children as compared to their interactions with the siblings of the ADHD children (Tarver-Behring et al., 1985).
It is the presence of comorbid ODD that is associated with the highest levels of interaction conflicts between parents and their ADHD children and adolescents (Barkley, Anastopoulos, et al., 1992; Barkley, Fischer, et al., 1992; Edwards et al., 2001; Johnston, 1996; Johnston & Mash, 2001). In a sequential analysis of these parent-teen interaction sequences, investigators have noted that it is the immediate or first lag in the sequence that is most important in determining the behavior of the other member of the dyad (Fletcher, Fischer, Barkley, & Smallish, 1996). That is, the behavior of each member is determined mainly by the immediately preceding behavior of the other member and not by earlier behaviors of either member in the chain of interactions. The interactions of the comorbid ADHD/ODD group reflected a strategy best characterized as “tit for tat” in that the type of behavior (positive, neutral, or negative) of each member was most influenced by the same type of behavior emitted immediately preceding it. Mothers of ADHD only and normal teens were more likely to utilize positive and neutral behaviors regardless of the immediately preceding behavior of their teens, characterized as a “be nice and forgive” strategy that is thought to be more mature and more socially successful for both parties in the long run (Fletcher et al., 1996). Even so, those with ADHD alone are still found to be deviant from normal in these interaction patterns even though less so than the comorbid ADHD/ODD group. The presence of comorbid ODD has also been shown to be associated with greater maternal stress and psychopathology as well as marital difficulties (Barkley, Anastopoulos, et al., 1992; Barkley, Fischer, et al., 1992; Johnston & Mash, 2001).
These interaction conflicts in families with ADHD children are not limited to just parent-child interactions. Increased conflicts have been observed between ADHD children and their siblings relative to normal child-sibling dyads (Mash & Johnston, 1983a; Taylor et al., 1991). Research on the larger domain of family functioning has shown that parents of ADHD children experience more parenting stress and decreased sense of parenting competence (Fischer, 1990; Johnston & Mash, 2001; Mash & Johnston, 1990; Theule et al., 2010), increased alcohol consumption in parents (Cunningham, Benness, & Siegel, 1988; Pelham & Lang, 1993), decreased extended family contacts (Cunningham et al., 1988), and increased marital conflict, separations, and divorce as well as maternal depression (Befera & Barkley, 1984; Cunningham et al., 1988; Barkley, Fischer, et al., 1990; Johnston & Mash, 2001; Lahey et al., 1988; Taylor et al., 1991). Again, it is the comorbid association of ADHD with ODD, or CD, that is linked to even greater degrees of parental psychopathology, marital discord, and divorce than in ADHD-only children (Barkley, Fischer, et al., 1990, 1991; Lahey et al., 1988; Taylor et al., 1991). Interestingly, Pelham and Lang (1993) have shown that the increased alcohol consumption in these parents is, in part, directly a function of the stressful interactions they have with their ADHD children.
Research has demonstrated that the primary direction of effects within these interactions is from child to parent (Danforth et al., 1991; Johnston & Mash, 2001; Mash & Johnston, 1990) rather than the reverse. That is, much of the disturbance in the interaction seems to stem from the effects of the child’s excessive, impulsive, unruly, noncompliant, and emotional behavior on the parent rather than from the effects of the parent’s behavior on the child. This was documented primarily through studies that evaluated the effects of stimulant medication on the behavior of the children and their interaction patterns with their mothers. Such research found that medication improves the compliance of those with ADHD and reduces their negative, talkative, and generally excessive behavior such that their parents reduce their levels of directive and negative behavior as well (Barkley & Cunningham, 1979b; Barkley, Karlsson, Pollard, & Murphy, 1985; Danforth et al., 1991; Humphries, Kinsbourne, & Swanson, 1978). These effects of medication are noted even in the preschool-aged group of children with ADHD (Barkley, 1988) as well as in those in late childhood (Barkley et al., 1985), and in both genders of ADHD children (Barkley, 1989b). Besides a general reduction in the negative, disruptive, and conflictual interaction patterns of these children with parents resulting from stimulant medication, general family functioning also seems to improve when ADHD children are treated with stimulant medication (Schachar, Taylor, Weiselberg, Thorley, & Rutter, 1987). None of this is to say that parental reactions to disruptive child behavior, parental skill and competence in child management and daily rearing, and parental psychological impairment are unimportant influences on children with ADHD. Evidence certainly shows that parental management, child monitoring, parental antisocial activity, maternal depression, father absence, and other parent and family factors are exceptionally important in the development of ODD, CD, major depression, and other disorders likely to be comorbid with ADHD (Johnson, Cohen, Kasen, Smailes, & Brook, 2001; Johnston & Mash, 2001; Pfiffner, McBurnett, & Rathouz, 2001; Patterson et al., 2000). But it is to say, as the behavioral genetic studies below will strongly attest, that these are not the origins of the child’s impulsive, hyperactive, and inattentive behavior and the related deficits in executive functioning and self-regulation.
More recent research shows that some degree of the family conflicts in children with ADHD also results from the fact that their parents are more likely to have ADHD and that parental ADHD can interfere with typical parenting behavior, whether or not the child has ADHD (Johnston et al., 2012). Parents with ADHD are less attentive and rewarding, more negative, and monitor their children less than do typical parents.
The patterns of disruptive, intrusive, excessive, negative, and emotional social interactions of ADHD children noted above in parent-child relations have been found to occur in their interactions with teachers (Whalen, Henker, & Dotemoto, 1980). It should come as no surprise, then, that those with ADHD receive more correction, punishment, censure, and criticism from their teachers than other children, as well as more school suspensions and expulsions, particularly if they have ODD/CD (Barkley et al., 1990; Whalen et al., 1980).
In their social relationships, ADHD children experience substantial difficulties (Clark, Cheyne, Cunningham, & Siegel, 1988; Cunningham & Siegel, 1987; DuPaul et al., 2001; Hoza, 2007; Nijmeijer et al., 2008; Whalen, Henker, Collins, McAuliffe, & Vaux, 1979). They are less liked by other children, have fewer friends, and are overwhelmingly rejected as a consequence (Erhardt & Hinshaw, 1994), particularly if they have comorbid conduct problems (Gresham, MacMillan, Bocian, Ward, & Forness, 1998; Hinshaw & Melnick, 1995). Indeed, among such comorbid cases, up to 70% may be rejected by peers and have no reciprocated friendships by 4th grade (Gresham et al., 1998). These peer relationship problems are not only the result of the more active, talkative, and impulsive actions of ADHD children, but are also a consequence of their greater emotional, facial, tonal, and bodily expressiveness, particularly anger, and more limited reciprocity in interactions, use of fewer positive social statements, more limited knowledge of social skills, and more negative physical behavior (Casey, 1996; Erhardt & Hinshaw, 1994; Grenel, Glass, & Katz, 1987; Madan-Swain & Zentall, 1990). Those with ODD/CD also prefer more sensation-seeking, fun-seeking, and trouble-seeking activities that further serve to alienate their normal peers (Hinshaw & Melnick, 1995; Melnick & Hinshaw, 1996; Nijmeijer et al., 2008). ADHD children seem to process social and emotional cues from others in a more limited and error-prone fashion, as if they were not paying as much attention to emotional information provided by others. Yet they do not differ in their capacity to understand the emotional expressions of other children (Casey, 1996). However, in those with comorbid ODD/CD, there may be a greater misperception of anger and a greater likelihood of responding with anger and aggression to peers than normal children (Cadesky, Mota, & Schachar, 2000; Casey, 1996; Matthys, Cuperus, & van Engeland, 1999). Little wonder then that ADHD children perceive themselves as receiving less social support from peers (and teachers) than do normal children (Demaray & Elliott, 2001). The problems with aggression and poor emotion regulation are also evident in the sports behavior of ADHD children with their peers (Johnson & Rosen, 2000). Once more, stimulant medication has been observed to decrease these negative and disruptive behaviors toward teachers (Whalen et al., 1980) and peers (Cunningham, Siegel, & Offord, 1985; Wallander, Schroeder, Michelli, & Gualtieri, 1987; Whalen et al., 1987) but may not result in any increase in more prosocial or positive initiatives toward peers (Wallander et al., 1987).
The postnatal course of those with hyperactivity has been shown to be subject to more stress and complications in several studies (Hartsough & Lambert, 1985; Stewart et al., 1966; Taylor et al., 1991). Chronic health problems, such as recurring upper respiratory infections, asthma, and allergies, have also been documented in the later preschool and childhood years of hyperactive children (Hartsough & Lambert, 1985; Mitchell, Aman, Turbott, & Manku, 1987; Szatmari et al., 1989). And, children with atopic (allergic) disorders have been shown to have more symptoms of ADHD (Roth, Beyreiss, Schlenzka, & Beyer, 1991). Yet, more careful research using better control groups, longitudinal samples, or analysis of the familial aggregation of disorders has not shown a specific association of these disorders with hyperactivity (Biederman, Milberger, Faraone, Guite, & Warburton, 1994; McGee, Stanton, & Sears, 1993; Mitchell et al., 1987; Taylor et al., 1991).
One study suggests that ADHD may be associated with growth deficits, particularly in height, during late childhood and early adolescence (Faraone et al., 2011; Spencer et al., 1996) while being associated with the opposite pattern in younger children (Faraone et al., 2011). These deficits did not exist in older adolescents, suggesting that the problem with growth is one of delayed maturation.
In one of the first studies of the issue, Stewart and colleagues (Stewart, Pitts, Craig, & Dieruf, 1966) found four times more hyperactive children to be described by parents as accident-prone compared to control children (43% vs 11%). Later studies have also identified such risks, with up to 57% of hyperactive or ADHD children said to be accident-prone by parents relative to 11% or fewer of control children (Barkley, 2006; Mitchell, Aman, Turbott, & Manku, 1987; Reebye, 1997). Interestingly, knowledge about safety does not appear to be lower in overactive, impulsive children than in control children. And so simply teaching more knowledge about safety may not suffice to reduce the accident risks of hyperactive children (Mori & Peterson, 1995).
Most studies find that ADHD children experience more injuries of various sorts than control children (Barkley, 2006) and that children experiencing injuries are more likely to manifest ADHD symptoms (Karaszia et al., 2011). In one study, 16% of their hyperactive sample had at least four or more serious accidental injuries, such as broken bones, lacerations, head injuries, severe bruises, lost teeth, etc., compared to just 5% of control children (Hartsough & Lambert, 1986). Jensen and colleagues (Jensen, Shervette, Xenakis, & Bain, 1988) found that 68% of ADD children, compared to 39% of control children, had experienced physical trauma sufficient to warrant sutures, hospitalization, or extensive/painful procedures. Several other studies likewise found a greater frequency of accidental injuries than among control children (Taylor, Sandberg, Thorley, & Giles, 1991), as did I when I analyzed data from research by Terri Shelton and I (Shelton et al., 1998) and found that more than four times as many had an accident related to their impulsive behavior (28.4% vs. 6.4%) than did control children. Recent research shows a greater risk for pedestrian injuries in children with ADHD that seems related to poor concern for safety in traffic situations, such as in choosing when and where to cross roadways (Stavrinos et al., 2011).
Head trauma may not be over-represented among hyperactive or ADHD children in some studies (Stewart et al., 1966; Szatmari et al., 1989). As for burns, only one study of ADHD children has been done and it did not find a significantly elevated incidence (2.0% vs. 2.4% for controls) (Szatmari et al., 1989). Bone fractures, in contrast, seem to be somewhat more common in ADHD than control children (23.5% vs. 15.1%) (Szatmari et al., 1989). ADHD children may be two to three times more likely to experience accidental poisonings (21% vs. 8% in Stewart, Thach, and Freidin, 1970; 7% vs. 3% in Szatmari, Offord, & Boyle, 1989). Jensen and colleagues (Jensen et al., 1988) found 13% of ADD children and 8% of control children had ingested poisonous substances.
The most extensively studied form of accidents occurring among those with hyperactivity or ADHD is motor vehicle crashes (Barkley & Cox, 2007). Evidence emerged years ago that hyperactive children, as teens, had a higher frequency of vehicular crashes as the driver than control subjects (1.3 vs. .07, p<.05) (Weiss & Hechtman, 1993). Also noteworthy in their driving histories was a significantly greater frequency of citations for speeding (Barkley & Cox, 2007).
Subsequently, my colleagues and I (Barkley, Guevremont, Anastopoulos, DuPaul & Shelton, 1993) found that ADHD teens had more crashes as the driver (1.5 vs. 0.4) than did control teens over their first few years of driving. Forty percent of the ADHD group had experienced at least two or more such crashes relative to just 6% of the control group. Four times more ADHD teens were deemed to have been at fault in their crashes as the driver than control teens (48.6% vs. 11.1%) and were at fault more frequently than the controls (0.8 vs. 0.4). In keeping with the Weiss and Hechtman (1993) initial report, ADHD teens were more likely to get speeding tickets (65.7% vs. 33.3%) and got them more often (Means=2.4 vs. 0.6). Two studies in New Zealand using community samples suggest a similarly strong relationship between ADHD and vehicular accident risk (Nada-Raja, Langley, McGee, Williams, Begg, & Reeder, 1997; Woodward, Fergusson, & Horwood, 2000). Adults diagnosed with ADHD also manifest more unsafe motor vehicle operation and crashes. (Barkley & Cox, 2007; Barkley et al., 2008). For instance, in one study more ADHD adults have their licenses suspended (24% vs. 4.0%) than in the control group and reported having received more speeding tickets (Means=4.9 vs. 1.1) than control adults (Murphy & Barkley, 1996). The difference in the frequency of vehicular crashes between the groups was only marginally significant (Means=2.8 vs. 1.8, p<.06), however.
Later, in a more thorough examination of driving (Barkley, Murphy, & Kwasnik, 1996b), we found that the ADHD group reported having had more vehicular crashes (Means=2.7 vs. 1.6), and a larger proportion of the ADHD group had been involved in more severe crashes (resulted in injuries) than were the control subjects (60% vs. 17%). Again, speeding citations were over-represented in their self-reports (100% vs. 56%) and occurred more frequently in the ADHD than control groups (means=4.9 vs. 1.3).
The most thorough study to date of driving performance among ADHD young adults (Barkley, Murphy, DuPaul, & Bush, 2002) used a multi-method, multi-source battery of measures. More than twice as many ADHD young adults had been involved in three or more vehicular crashes as the driver than had members of the control group (26% vs. 9%) and had been held at fault in three or more such crashes (7% vs. 3%). The ADHD group had been involved in more vehicular crashes than the control adults (Means=1.9 vs. 1.2) and had been held to be at fault in more crashes (means=1.8 vs. 0.9). The dollar damage caused in their first accidents was estimated to be more than twice as high in the ADHD group than the control group (Means=$4221 vs. $1665). As in the earlier studies, the ADHD group reported a greater frequency of speeding citations (3.9 vs. 2.4) and a higher percentage had had their licenses suspended than in the control group (22%vs. 5%). Both the greater frequency of speeding citations and license suspensions were corroborated through the official state driving records for these young adults.
These studies leave little doubt that ADHD, or its symptoms of inattention and hyperactive-impulsive behavior, are associated with a higher risk for unsafe driving and motor vehicle accidents than in the normal population (Barkley & Cox, 007; Barkley et al., 2008). In view of the substantial costs that must be associated with such a higher rate of adverse driving outcomes, prevention and intervention efforts are certainly called for to attempt to reduce the driving risks among those having ADHD.
Many studies have suggested an association between ADHD and sleep disturbances (Barkley, 2006; Ball, Tiernan, Janusz, & Furr, 1997; Cortese et al., 2009; Gruber, Sadeh, & Raviv, 2000; Kaplan, McNichol, Conte, & Moghadam, 1987; Stewart et al., 1966; Trommer, Hoeppner, Rosenberg, Armstrong, & Rothstein, 1988; Wilens, Biederman, & Spencer, 1994). Perhaps half of these problems are mainly more behavioral problems at bedtime, but there is evidence that a significant minority of children with ADHD take a longer time to fall asleep, show greater instability of sleep duration, tiredness at awakening, or frequent night waking (Cortese et al., 2009). For instance, Stein (1999) evaluated 125 psychiatrically diagnosed children with 83 pediatric outpatient children and found moderate to severe sleep problems in 19% of those with ADHD, 13% of the psychiatric controls, and 6% of pediatric outpatients. Treatment with stimulant medication increased the proportion of ADHD children with sleep problems to 29%, a not unexpected finding given the well-known stimulant side effect of increased insomnia (see Barkley, 1998). Sleep EEGs have typically not revealed differences in the quality of sleeping, however (Ball & Kolonian, 1995). Other research implies that it may be the comorbid disorders (ODD, anxiety disorders, etc.) associated with ADHD that contribute to the increased risk for some of these sleep problems (Corkum, Beig, Tannock, & Modolfsky, 1997). Indeed, a later study by Corkum and associates found that sleep problems occurred twice as often in ADHD than in control children. These problems could be reduced to three general factors: (1) dyssomnias (bedtime resistance, sleep onset problems, or difficulty arising), (2) sleep-related involuntary movements (teeth grinding, sleeptalking, restless sleep, etc.), and (3) parasomnias (sleepwalking, night wakings, sleep terrors). Dyssomnias were primarily related to comorbid ODD or treatment with stimulant medication, while parasomnias were not significantly different from the control group. However, involuntary movements were significantly elevated in children with the Combined Type of ADHD (Corkum, Moldofsky, Hogg-Johnson, Humphries, & Tannock, 1999).
Within normal populations, quantity of sleep is inversely associated with an increased risk for school behavioral problems (Aronen, Paavonen, Fjallnerg, Soinen, & Torronen, 2000), particularly daytime sleepiness and inattention rather than hyperactive-impulsive behavior (Fallone, Acebo, Arnedt, Seifer, & Carskadon, 2001). The direction of effect, then, between ADHD and sleep problems is unclear. It is possible that sleep difficulties increase ADHD symptoms during the daytime, as the research on normal children implies. Yet, some research finds that the sleep problems of ADHD children are not associated with the severity of their symptoms, suggesting that it is the disorder, not the impaired sleeping, that contributes to impaired daytime alertness, inattention, and behavioral problems (Lecendreau, Konofal, Bouvard, Falissard, & Mouren-Simeoni, 2000).
Considerable research has accumulated on various etiologies for ADHD (Barkley, 2006; Nigg, 2006). Notably, virtually all of this research pertains to the DSM-IV Combined Type of ADHD or what was previously considered hyperactivity in children. Readers should not extend these findings to the other attention disorder noted above to have sluggish cognitive tempo that is likely a qualitatively different disorder. But for ADHD, there is even less doubt now among career investigators in this field that, while multiple etiologies may lead to ADHD, neurological and genetic factors likely play the greatest role in causing this disorder. These two areas, along with the associated field of the neuropsychology of ADHD, have witnessed enormous growth in the past decade, further refining our understanding of the neuro-genetic basis of the disorder. Our knowledge of the final common neurological pathway through which these causes produce their effects on behavior has become clearer from converging lines of evidence employing a wide array of assessment tools, including neuropsychological tests sensitive to frontal lobe functioning, electrophysiological measures (EEG, QEEG, ERP), measures of cerebral blood flow, and neuro-imaging studies using positron emission tomography (PET), magnetic resonance imaging (MRI), and functional MRI. Several recent studies have even identified specific protein abnormalities in specific brain regions that may be linked to possible neurochemical dysregulation in the disorder. Precise neurochemical abnormalities that may underlie this disorder have proven extremely difficult to document with any certainty over the past decade, but advancing psychopharmacological, neurological, as well as genetic evidence suggests involvement in at least two systems, these being dopaminergic and noradrenergic. Neurological evidence has converged on the brain networks involved in ADHD, as discussed below. Whereas most early findings on etiologies were correlational in nature, not permitting direct, precise, immediate molecular evidence of primary causality, more recent evidence in this past decade has provided the confirmatory evidence of precisely which brain regions and their networks are creating the symptoms of ADHD.
A variety of neurological etiologies have been proposed for ADHD. Brain damage was initially proposed as an initial and chief cause of ADHD symptoms (Still, 1902), either occurring as a result of known brain infections, trauma, or other injuries or complications occurring during pregnancy or at the time of delivery (see Barkley, 2006, for more on the History of ADHD, and more recently Barkley & Peters, 2012). Several studies show that brain damage, particularly hypoxic/anoxic types of insults, is associated with greater attention deficits and hyperactivity (Cruikshank, Eliason, & Merrifield, 1988; O'Dougherty, Nuechterlein, & Drew, 1984). ADHD symptoms also occur more in children with seizure disorders (Holdsworth & Whitmore, 1974) that are clearly related to underlying neurological malfunction. However, most ADHD children have no history of significant brain injuries or seizure disorders, and so brain damage is unlikely to account for the majority of children with ADHD (Rutter, 1977).
Throughout the century, investigators have repeatedly noted the similarities between symptoms of ADHD and those produced by lesions or injuries to the frontal lobes more generally and the prefrontal cortex specifically (Barkley, 1997b; Benton, 1991; Heilman, Voeller, & Nadeau, 1991; Levin, 1938; Mattes, 1980). Both children and adults suffering injuries to the prefrontal region demonstrate deficits in sustained attention, inhibition, regulation of emotion and motivation, and the capacity to organize behavior across time (Barkley, 2010, 2012; Fuster, 1997; Grattan & Eslinger, 1991; Stuss & Benson, 1986).
Much of the neuropsychological evidence pertaining to ADHD was reviewed above under the particular forms of cognitive impairment seen in ADHD. A large number of studies have used neuropsychological tests of frontal lobe functions and have detected deficits on these tests, albeit inconsistently (Frazier et al., 2004; Heavey et al., 2004; Willcutt et al., 2010). Results suggest that it is poor inhibition of behavioral responses, or what Nigg (2001, 2006) has called executive inhibition, that is solidly established as impaired in this disorder. As noted earlier, evidence also exists for related difficulties as well, with nonverbal and verbal working memory, planning, verbal fluency, response perseveration, motor sequencing, sense of time, and other frontal lobe functions (Willcutt et al., 2005). Adults with ADHD have also been shown to display similar deficits on neuropsychological tests of executive functions (Barkley et al., 2008;Frazier et al., 2004). One recent study of adults also found diminished olfactory identification in adults with ADHD, a finding predicted on the basis that both executive functions and olfactory identification are mediated by prefrontal regions (Murphy et al., 2001). Moreover, research shows that not only do siblings of ADHD children who have ADHD show similar executive function deficits, but even those siblings of ADHD who do not actually manifest ADHD appear to have milder yet significant impairments in these same executive functions (Seidman, Biederman, Weber, Monuteaux, & Faraone, 1997). Such findings imply a possible genetically linked risk for executive function deficits in families having ADHD children, even if symptoms of ADHD are not fully manifest in those family members. Supporting this implication is evidence that the executive deficits in ADHD arise from the same substantial shared genetic liability as do the ADHD symptoms themselves and as does the overlap of ADHD with ODD/CD (Coolidge, Thede, & Young, 2000). Important in recent studies in this area has been the demonstration that these inhibitory and executive deficits are not the result of comorbid disorders, such as ODD, CD, anxiety, or depression, thus giving greater confidence to their affiliation with ADHD itself (Barkley, Edwards et al., 2001; Barkley, Murphy et al., 2001; Bayliss & Roodenrys, 2000; Chang et al., 1999; Clark, Prior, & Kinsella, 2000; Klorman et al., 1999; Murphy et al., 2001; Nigg et al., 1998; Oosterlaan, Scheres, & Sergeant, 2002; Wiers, Gunning, & Sergeant, 1998). This is not to say that some other disorders, such as learning disabilities or autism, do not affect some executive functions (Barkley, 2012e), such as those of verbal working memory, perhaps owing to their associated deficits in language development, but that the pattern of deficits associated with ADHD is not typical of these other disorders (Pennington & Ozonoff, 1996). The totality of findings in the neuropsychology of ADHD is impressive in further suggesting that some dysfunction of the prefrontal lobes (inhibition and executive function deficits) is involved in this disorder. Despite such findings, only 35% to 50% of children or adults with ADHD are likely to fall in the impaired range on various tests of EF but this rises to 86% to 98% of cases if rating scales of EF are employed (Barkley, 2011c). Since the ratings have far greater ecological validity than do the tests of EF, such evidence supports the assertion that ADHD is in fact a disorder of EF.
Early research in the 1960s and '70s focused on psychophysiological measures of nervous system (central and autonomic) electrical activity, variously measured (electroencephalograms, galvanic skin responses, heart rate deceleration, etc.). These studies were inconsistent in demonstrating group differences between ADHD and control children in resting arousal. But where differences from normal are found, they are consistently in the direction of diminished reactivity to stimulation, or arousability, in those with ADHD (see Hastings & Barkley, 1978, for an early review). Research continues to demonstrate differences in skin conductance and heart rate parameters in response to stimulation in those with ADHD (Borger & van der Meere, 2000) that may distinguish them from children with conduct disorder or those with comorbid ADHD/CD (Beaucheine et al., 2001; Herpertz, Wenning, Mueller, Qunaidi, Sass, & Herpertz-Dahlmann, 2001).
Far more consistent have been the results of quantitative electroencephalograph (QEEG) and evoked response potential (ERP) measures, sometimes taken in conjunction with vigilance tests (Frank, Lazar, & Seiden, 1992; Klorman, 1992; Klorman, Salzman, & Borgstedt, 1988; Rothenberger, 1995). Although results have varied substantially across these studies (see Loo & Barkley, 2005; Loo & Makieg, for reviews), the most consistent pattern for EEG research is increased slow wave, or theta, activity, particularly in the frontal lobe, and excess beta activity, all indicative of a pattern of under-arousal and under-reactivity in ADHD. ADHD children have been found to have smaller amplitudes in the late positive and negative components of their evoked response patterns (ERPs). These late components are believed to be a function of the prefrontal regions of the brain, are related to poorer performances on inhibition and vigilance tests, and are corrected by stimulant medication (Johnstone, Barry, & Anderson, 2001; Pliszka, Liotti, & Woldorff, 2000). Thus, psychophysiological abnormalities related to sustained attention and inhibition indicate an under-responsiveness of ADHD children to stimulation that is corrected by stimulant medication.
Several studies have also examined cerebral blood flow using single photon emission computed tomography (SPECT) in ADHD and normal children (see Hendren, DeBacker, & Pandina, 2000, Nigg, 2006, for reviews). They have consistently shown decreased blood flow to the prefrontal regions (most recently in the right frontal area) and pathways connecting these regions to the limbic system via the striatum and specifically its anterior region known as the caudate, and with the cerebellum. Degree of blood flow in the right frontal region has been correlated with behavioral severity of the disorder, while that in more posterior regions and the cerebellum seems related to degree of motor impairment (Gustafson et al., 2000).
Studies using positron emission tomography (PET) to assess cerebral glucose metabolism have found diminished metabolism in adults, particularly in the frontal region (Schweitzer, Faber, Grafton, Tune, Hoffman, & Kilts, 2000; Zametkin et al., 1990) and adolescent females with ADHD (Ernst et al., 1994) but have proven negative in adolescent males with ADHD (Zametkin et al., 1993). An attempt to replicate the finding with adolescent females having ADHD in younger female ADHD children failed to find such diminished metabolism (Ernst, Cohen, Liebenauer, Jons, & Zametkin, 1997). Such studies are plagued by their exceptionally small sample sizes that result in very low power to detect group differences and considerable unreliability in replicating previous findings. However, significant correlations have been noted between diminished metabolic activity in the anterior frontal region and severity of ADHD symptoms in adolescents with ADHD (Zametkin et al., 1993). Also, using a radioactive tracer that indicates dopamine activity, Ernst and colleagues were able to show abnormal dopamine activity in the right midbrain region of ADHD children and that severity of symptoms was correlated with the degree of this abnormality (Ernst, Zametkin, Matochik, Pascualvaca, Jons, & Cohen, 1999). These demonstrations of an association between the metabolic activity of certain brain regions and symptoms of ADHD and associated executive deficits is critical to proving a connection between the findings pertaining to brain activation and the behavior comprising ADHD.
Other neuro-imaging technologies offer a more fine-grained analysis of brain structures using the higher resolution magnetic resonance imaging (MRI) devices (Hart et al., 2012). Studies employing this technology find differences in selected brain regions in those with ADHD relative to control groups.
To date, at least five brain regions have been implicated in producing ADHD. These are the dorsolateral and orbital frontal regions, mainly on the right side, the anterior cingulated cortex, the basal ganglia, especially the striatum, the cerebellum (principally the vermis on the right side), and the anterior portion of the corpus callosum (the splenium) (Hart et al., 2012; Valera et al., 2007). The various brain regions often implicated in ADHD in the most recent MRI research are illustrated in Figure 1.1. Here the right hemisphere of the brain is shown but the left hemisphere has been cut away to expose the location of the striatum in relation to the prefrontal regions controlling movement specifically and behavior generally.
Figure 1.1 Diagram of the human brain showing the right hemisphere, and particularly the location of the caudate nucleus (striatum), globus pallidus, and cerebellar vermis. From R. A. Barkley (1998). Attention deficit hyperactivity disorder. Scientific American, September, p. 47. Reprinted with permission of the artist, Terese Winslow.
With the advent of even more advanced functional MRI technology, researchers can now evaluate functional activity in various brain regions while administering psychological tests to subjects being scanned. These studies find children and adults with ADHD to have abnormal patterns of activation during attention and inhibition tasks than do normal children, particularly in the right prefrontal region, basal ganglia (striatum and putamen), anterior cingulated, and the cerebellum (Nigg, 2006; Hart et al., 2012; Vaidya et al., 1998; Valera et al., 2007). Again, the demonstrated linkage of brain structure and function with psychological measures of ADHD symptoms and executive deficits is exceptionally important in such research to permit causal inferences to be made about the role of these brain abnormalities in the cognitive and behavioral abnormalities comprising ADHD.
Possible neurotransmitter dysfunction or imbalances have been proposed in ADHD for quite some time (see Sagvolden, 2005; Pliszka, McCracken, & Maas, 1996 for reviews). Initially, these rested chiefly on the responses of ADHD children to differing drugs. ADHD children respond remarkably well to stimulants, most of which act by increasing the availability of dopamine via various mechanisms, and producing some effects on the noradrenergic pathways as well (Connor, 2006). Consequently, it seemed sensible to hypothesize that these two neurotransmitters might be involved in the disorder. Given the findings that normal children show a positive, albeit lesser, response to stimulants (Rapoport et al., 1978), however, partially undermines this logic. Other, more direct evidence comes from studies of cerebral spinal fluid in ADHD and normal children that indicated decreased brain dopamine in ADHD children (Raskin, et al., 1984). Similarly, other studies used blood and urinary metabolites of brain neurotransmitters to infer deficiencies in ADHD, largely related to dopamine regulation. Early studies of this sort proved conflicting in their results (Shaywitz, Shaywitz, Cohen, & Young, 1983; Shaywitz, Shaywitz, Jatlow, et al., 1986; Zametkin & Rapoport, 1986). A subsequent study continued to find support for reduced noradrenergic activity in ADHD as inferred from significantly lower levels of a metabolite of this neurotransmitter (Halperin et al., 1997). What limited evidence there is from this literature seems to point to a selective deficiency in the availability of both dopamine and norepinephrine, but this evidence cannot be considered conclusive at this time. Far greater evidence for involvement of these and other neurotransmitters comes from the rapidly growing evidence for the role of gene polymorphisms involved in regulating these neurotransmitters that reveals different gene variations in ADHD than in typical population samples (for reviews, see Banaschewski et al., 2010; Smith et al., 2009; Wu et al., 2012).
Most studies have found a greater incidence of pregnancy or birth complications in ADHD compared to normal children (Hartsough & Lambert, 1985; Minde, Webb, & Sykes, 1968). Children born prematurely or who have markedly lower birth weights are at high risk for later inattention, hyperactivity or ADHD (Breslau et al., 1996; Groen-Blokhuis et al., 2012; Schothorst & Engeland, 1996; Sykes et al., 1997; Szatmari, Saigal, Rosenbaum, & Campbell, 1993). It is not merely low birth weight that seems to pose the risk for symptoms of ADHD or the disorder itself, among other psychiatric disorders, but the extent of white matter abnormalities due to birth injuries, such as parenchymal lesions and/or ventricular enlargement (Whittaker et al., 1997). These findings suggest that some cases of ADHD may arise from such complications, especially from prematurity associated with minor bleeding in the brain (Nigg, 2006).
Far more evidence exists for the role of exposure to various environmental toxins during pregnancy and a significantly elevated risk for ADHD, such as occurs in maternal smoking and alcohol consumption (Froehlich et al., 2011; Rodriguez et al., 2009). And recent studies suggest that it is the interaction of these substances with certain high risk genotypes for ADHD that further elevate the risk for the disorder (Altink et al., 2009; Neuman et al., 2012).
Evidence for a genetic basis to this disorder is now overwhelming (Banaschewski et al., 2010; Smith et al., 2009; Wu et al., 2012) and comes from four sources: family studies of the aggregation of the disorder among biological relatives, adoption studies, twin studies, and, most recently, molecular genetic studies identifying individual candidate genes.
For years, researchers have noted the higher prevalence of psychopathology in the parents and other relatives of children with ADHD. Between 10% to 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% (Biederman et al., 1992; Biederman, Faraone, Keenan, et al., 1990; Nigg, 2006; Pauls, 1991; Welner et al., 1977). Even more striking, research shows that if a parent has ADHD, the risk to the offspring is 40% to 57% (Barkley et al., 2008; Biederman, Faraone, Mick, et al., 1995). Thus, ADHD clusters significantly among the biological relatives of children or adults with the disorder, strongly indicating a hereditary basis to this condition. Subsequently, these elevated rates of disorders also have been noted in African-American ADHD samples (Samuel et al., 1999) as well as in ADHD girls compared to boys (Faraone et al., 2000).
These studies of families further suggest that ADHD with CD may be a distinct familial subtype of ADHD. By separating the group of ADHD children into those with and without conduct disorder (CD), it has been shown that the conduct problems, substance abuse, and depression in the parents and other relatives are related more to the presence of CD in the ADHD children than to ADHD itself (August & Stewart, 1983; Biederman, Faraone, Keenan, et al., 1992; Faraone, Biederman, et al., 1995; Faraone, Biederman, Mennin, Russell, & Tsuang, 1998; Lahey et al., 1988; Waschbusch, 2002). Rates of hyperactivity or ADHD remain high even in relatives of the group of ADHD children without CD (Biederman, Faraone, Keenan, et al., 1992) but depression and antisocial spectrum disorders are most likely to appear in the comorbid group. Using sib-pairs in which both siblings had ADHD, Smalley and colleagues have also supported this view through findings that CD significantly clusters among the families of only those sib-pairs having CD (Smalley et al., 2000).
Some research has also suggested that girls who manifest ADHD may need to have a greater genetic loading (higher family member prevalence) than do males with ADHD (Smalley et al., 2000). Faraone and colleagues also found some evidence in support of this view in that male siblings from families with one affected child were more likely to have ADHD than were female siblings from these families (Faraone et al., 1995). They also reported that the gender difference noted above for ADHD children (3:1 males-to-females) may apply primarily to children from families in which either the child or a parent has antisocial behavior.
Interestingly, research by Faraone and Biederman (1997) suggests that depression among family members of children with ADHD may be a nonspecific expression of the same genetic contribution that is related to ADHD. This is based on their findings that family members of children with ADHD are at increased risk for major depression while individuals having major depression have first-degree relatives at increased risk for ADHD. Even so, as noted above, the risk for depression among family members is largely among those children having ADHD with CD.
Another line of evidence for genetic involvement in ADHD has emerged from studies of adopted children. Early on, Cantwell (1975) and Morrison and Stewart (1973) both reported higher rates of hyperactivity in the biological parents of hyperactive children than in adoptive parents having such children. Both studies suggest that hyperactive children are more likely to resemble their biological parents than their adoptive parents in their levels of hyperactivity. Yet, both studies were retrospective and both failed to study the biological parents of the adopted hyperactive children as a comparison group (Pauls, 1991). Cadoret and Stewart (1991) studied 283 male adoptees and found that if one of the biological parents had been judged delinquent or to have an adult criminal conviction, the adopted away sons had a higher likelihood of having ADHD. A later study (van den Oord, Boomsma, & Verhulst, 1994) using biologically related and unrelated pairs of international adoptees identified a strong genetic component (47% of the variance) for the Attention Problems dimension of the Child Behavior Checklist, a rating scale commonly used in research on ADHD. More recently, a comparison of the families of adopted ADHD children to those living with their biological parents and to a control group also showed the same pattern of an elevated prevalence of ADHD among just the biological parents of the ADHD children (6% vs. 18% vs. 3% respectively) (Sprich, Biederman, Crawford, Mundy, & Faraone, 2000). Thus, like the family association studies discussed earlier, results of adoption studies point to a strong possibility of a significant hereditary contribution to hyperactivity.
The number of twin studies of ADHD and its underlying behavioral dimensions is now substantial (Nicholas & Burt, 2010; Nigg, 2006). There has been a striking consistency across all of these studies in the pattern of their results. This research strategy provides a third avenue of evidence for a genetic contribution to ADHD. But it also provides a means of testing any competing environmental theories of the disorder (e.g., that ADHD is due to poor parenting, adverse family life, excessive TV viewing, etc.). That is because twin studies can not only compute the proportion of variance in a trait that is genetically influenced (heritability), but also the proportion that results from common or shared environment (things twins and siblings have in common growing up in the same family) and that which results from unique environment (all non-genetic factors or events that are unique or specific to one child and not to others in the family) (Plomin, Defries, McClearn, & Rutter, 1997).
Early research on ADHD using twins looked only at twin concordance (likelihood of twins sharing the same disorder) and did not compute these estimates of heritability, shared, and unique environment. These early studies demonstrated a greater agreement (concordance) for symptoms of hyperactivity and inattention between monozygotic (MZ) compared to dizygotic twins (DZ) (O'Connor, Foch, Sherry, & Plomin, 1980; Willerman, 1973). Studies of very small samples of twins (Heffron, Martin, & Welsh, 1984; Lopez, 1965) found complete (100%) concordance for MZ twins for hyperactivity and far less agreement for DZ twins. For instance, Gilger, Pennington, and DeFries (1992) found that if one twin was diagnosed as ADHD, the concordance for the disorder was 81% in MZ twins and 29% in DZ twins. Sherman, McGue, and Iacono (1997) found that the concordance for MZ twins having ADHD (mother identified) was 67% versus 0% for DZ twins.
Many subsequent studies have computed heritability and environmental contributions to ADHD (Nicholas & Burt, 2010; Nigg, 2006). These twin studies have found a high degree of heritability for ADHD, ranging from .75 to .97 and averaging about .78. Thus, twin studies indicate that the average heritability of ADHD is approximately 0.73, being nearly that for human height (.80-.91) and higher than that found for intelligence (.55-.70). These studies consistently find little, if any, effect of shared (rearing) environment on the traits of ADHD while sometimes finding a small significant contribution for unique environmental events (Burt et al., 2012). In their totality, shared environmental factors seem to account for 0% to 6% of individual differences in the behavioral trait(s) related to ADHD.
The twin studies cited above have also been able to indicate the extent to which individual differences in ADHD symptoms are the result of nonshared (unique) environmental factors. Such factors not only include those typically thought of as involving the social environment, but also all biological factors that are nongenetic in origin. Factors in the nonshared environment are those events or conditions that will have uniquely affected only one twin and not the other. Besides biological hazards or neurologically injurious events that may have befallen only one member of a twin pair, the nonshared environment also includes those differences in the manner in which parents may have treated each child. Parents do not interact with all of their children in an identical fashion and such unique parent-child interactions are believed to make more of a contribution to individual differences among siblings than do those factors about the home and child-rearing that are common to all children in the family. Twin studies to date have suggested that approximately 9% to 20% of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be attributed to such nonshared environmental (nongenetic) factors (Nicholas & Burt, 2010; Nigg, 2006). A portion of this variance, however, must be attributed to the error of the measure used to assess the symptoms. Research suggests that the nonshared environmental factors also contribute disproportionately more to individual differences in other forms of child psychopathology than do factors in the shared environment (Pike & Plomin, 1996). Thus, if researchers were interested in identifying environmental contributors to ADHD, these studies suggest that such research should focus on those biological and social experiences that are specific and unique to the individual and are not part of the common environment to which other siblings have been exposed.
Most investigators now accept the fact that multiple genes contribute to the disorder, given the complexity of the traits underlying ADHD and their dimensional nature (Banaschewski et al., 2010; Smith et al., 2009; Nigg, 2006; Wu et al., 2012). At least 45 sites or more in the human genome have been implicated in the risk for ADHD based on reviews of genome-wide scans today (Franke et al., 2009; Poelmans et al., 2011). Among these, an abundant literature demonstrates a considerable role for the DAT1 (dopamine transporter) and DRD4 (dopamine receptor density) genes.
As the twin and quantitative genetic studies have suggested, unique environmental events may play some role in individual differences in symptoms of ADHD (Nigg, 2006). This should not be taken to mean only those social factors within the realm of psychosocial or family influences. As noted above, variance in the expression of ADHD that may be due to environmental sources comprises all non-genetic sources more generally. These include pre-, peri-, and post-natal complications, and malnutrition, diseases, trauma, toxin exposure, and other neurologically compromising events that may occur during the development of the nervous system before and after birth. Evidence clearly suggests that most of these unique events or influences are likely to be various biologically compromising events. Several have been repeatedly linked to risks for inattention and hyperactive behavior.
One such factor is exposure to environmental toxins, specifically lead. Elevated body lead burden has been shown to have a small but consistent and statistically significant relationship to the symptoms comprising ADHD (Baloh, Sturm, Green, & Gleser, 1975; David, 1974; de la Burde & Choate, 1972, 1974; Needleman et al, 1979; Needleman et al., 1990; Nigg, 2006). However, even at relatively high levels of lead, less than 38% of children are rated as having the behavior of hyperactivity on a teacher rating scale (Needleman et al., 1979) implying that most lead poisoned children do not develop symptoms of ADHD. And most ADHD children, likewise, do not have significantly elevated lead burdens, although one study indicates their lead levels may be higher than in control subjects (Eskinazi & Gittelman, 1983). Studies which have controlled for the presence of potentially confounding factors in this relationship have found the association between body lead (in blood or dentition) and symptoms of ADHD to be .10-.19 with the more factors controlled, the more likely the relationship falls below .10 (Ferguson, Ferguson, Horwood, & Kinzett, 1988; Silva, Hughes, Williams, & Faed, 1988; Thompson et al., 1989). Only 4% or less of the variance in the expression of these symptoms in children with elevated lead is explained by lead levels. Moreover, two serious methodological issues plague even the better conducted studies in this area: (1) None of the early studies have used clinical criteria for a diagnosis of ADHD to determine precisely what percentage of lead-burdened children actually have the disorder – all have simply used behavior ratings comprising only a small number of items of inattention or hyperactivity; and (2) none of the early studies assessed for the presence of ADHD in the parents and controlled its contribution to the relationship. Given the high heritability of ADHD, this factor alone could attenuate the already small correlation between lead and symptoms of ADHD by as much as a third to a half of its present levels.
Other types of environmental toxins found to have some relationship to inattention and hyperactivity are prenatal exposure to alcohol and tobacco smoke (see Nigg, 2006 for a review; also Altink et al., 2009, Neuman et al., 2012; Rodriguez et al., 2009)). It has also been shown that parents of children with ADHD do consume more alcohol and smoke more tobacco than control groups even when not pregnant. Thus, it is reasonable for research to continue to pursue the possibility that these environmental toxins may be causally related to ADHD. However, as in the lead studies discussed above, most of the early research in this area suffered from the same two serious methodological limitations – the failure to utilize clinical diagnostic criteria to determine rates of ADHD in exposed children and the failure to evaluate and control for the presence of ADHD in the parents. More recent studies have addressed those concerns yet continue to show some relationships between these toxins and ADHD.
A few environmental theories of ADHD were proposed more than 30 years ago (Block, 1977; Willis & Lovaas, 1977) but have not received support in the available literature since then. Willis and Lovaas (1977) claimed that hyperactive behavior was the result of poor stimulus control by maternal commands and that this poor regulation of behavior arose from poor parental management of the children. Others have also conjectured that ADHD results from difficulties in the parents’ over-stimulating approach to caring for and managing the child, as well as parental psychological problems (Carlson, Jacobvitz, & Sroufe, 1995; Jacobvitz & Sroufe, 1987; Silverman & Ragusa, 1992). But these conjectures have not articulated just how deficits in behavioral inhibition, executive functioning, and other cognitive deficits commonly associated with clinically diagnosed ADHD as described above could arise purely from such social factors. Nor is it at all obvious how such factors could lead to the substantial evidence now accumulated on the deficiencies in brain development and functioning associated with ADHD, not to mention the striking role of heredity and molecular genetics in the disorder that demonstrate ADHD to be among the most genetically influenced of all mental disorders. Moreover, many of these early studies proclaiming to have evidence of parental characteristics as potentially causative of ADHD have not used clinical diagnostic criteria to identify their children as ADHD, instead relying merely on elevated parental ratings of hyperactivity or laboratory demonstrations of distractibility to classify the children as ADHD (Carlson et al., 1995; Silverman & Ragusa, 1992). Nor have these purely social theories received much support in the available literature that has studied clinically diagnosed children with ADHD (see Danforth et al., 1991; Johnston & Mash, 2001). The conclusion of the literature to date is that ADHD is likely to interfere with social relationships in both affected children and affected adults but that the disorder does not arise from such social relationships.
In view of the twin studies discussed above that show minimal, nonsignificant contributions of the common or shared environment to the expression of symptoms of ADHD, theories based entirely on social explanations of the origins of ADHD are difficult to take seriously any longer. This is not to say that the family and larger social environment do not matter, for they surely do. Despite the large role heredity seems to play in ADHD symptoms, they remain partly malleable to unique environmental influences and nonshared social learning. The types of comorbid disorders that will develop, the peer relationship problems that may arise, and various outcome domains impaired by the disorder are likely to be related in varying degrees to parent, family, and larger social factors (Johnson, Cohen, Kasen, Smailes, & Brook, 2001; Johnston & Mash, 2001; Milberger, 1997; Nigg, 2006; Pfiffner, McBurnett, &Rathouz, 2001; van den Oord & Rowe, 1997). Yet even here, care must be taken in interpreting these findings as evidence of a purely social contribution to such conditions that may be associated with ADHD. This is because many measures of family functioning and adversity also show a strong heritable contribution to them, largely owing to the presence of similar symptoms and disorders (and genes!) in the parents as may be evident in the child (Pike & Plomin, 1996; Plomin, 1995). Thus, there is a genetic contribution to the family environment; a fact that often goes overlooked in studies of family and social factors involved in ADHD.
It should be evident from the research reviewed here that ADHD arises from multiple etiologies, neurological and genetic factors being substantial ones. Like Nigg (2006) and Taylor (1999), I envision ADHD as having a heterogeneous etiology with various developmental pathways leading to this behavioral syndrome. These various etiologies and pathways, however, may give rise to the disorder through disturbances in a final common pathway in the nervous system. That pathway appears to be the integrity of the prefrontal cortical-striatal-cerebellar networks. It now appears that hereditary factors play the largest role in the occurrence of ADHD symptoms in children. It may be that what is transmitted genetically is a tendency toward smaller and less active or even defective prefrontal-striatal-cerebellar networks. The condition can also be caused or exacerbated by pregnancy complications, exposure to toxins, or neurological disease. Social factors alone cannot be supported as causal of this disorder but such factors may contribute to its persistence, and, more likely, contribute to the forms of comorbid disorders and the domains of impairment associated with ADHD. Cases of ADHD can also arise without a genetic predisposition to the disorder provided the child is exposed to significant disruption or neurological injury to this final common neurologic pathway, but this would seem to account for only a small minority of ADHD children. In general, then, research conducted since the last edition of this course has further strengthened the evidence for genetic and developmental neurological factors as likely causal of this disorder while greatly reducing the support for purely social or environmental factors as having a role.
Research continues to support the idea that a separate disorder of attention exists besides that seen in ADHD and that it may overlap in nearly half of all cases with the Predominantly Inattentive Presentation of ADHD (IP). Such children and adults having SCT differ in many important respects from children and adults with the more typical Combined Presentation (CP) of the disorder. Children with CP manifest more oppositional and aggressive symptoms, a greater likelihood of having ODD and CD, and more peer rejection than SCT children (Barkley,2012a, 2012b; Crystal et al., 2001; Milich et al., 2001; Penny et al., 2010; Willcutt et al., 1999). Those with SCT also may have a qualitatively different impairment in attention (selective attention and speed of information processing) (see Milich et al., 2001 for a thorough review). More than twice as many CP children than SCT cases may be diagnosed as Oppositional Defiant Disorder (41% vs. 19%), using DSM-III-R criteria, and more than three times as many as having Conduct Disorder (21% vs. 6%) (Barkley, DuPaul, & McMurray, 1990). The CP children may also be more likely to have speech and language problems (Cantwell & Baker, 1992). The CP children are described as more noisy, disruptive, messy, irresponsible, and immature. In contrast, children with SCT are characterized as more daydreamy, hypoactive, passive, apathetic, lethargic, confused, withdrawn, and sluggish (Barkley, 2012a, 2012b; McBurnett, Pfiffner, & Frick, 2001; Milich et al., 2001; Penny et al., 2010). Research suggests that these symptoms of SCT form two separate dimensions of inattention from that associated with ADHD in the DSM-IV and now DSM-5 (Barkley, 2011b, 2012a, 2012b; McBurnett et al., 2001; Penney et al., 2009). A study by Carlson and Mann (2002) indicates that if cases of SCT children are separated from other IP (ADHD) cases in children, then greater problems with anxiety/depression, social withdrawal, and general unhappiness and fewer problems with externalizing symptoms may be more evident in this SCT condition.
Social passivity and withdrawal have been repeatedly noted in other studies of SCT children (Maedgen & Carlson, 2000; Milich et al., 2001; Penney et al., 2009). Direct observations of the peer interactions of these subtypes tend to corroborate these ratings, finding that CP (ADHD) children are more prone to fighting and arguing whereas SCT children are more shy (Hodgens, Cole, & Boldizar, 2000).
More telling of the distinctiveness of these two attention disorders has been recent evidence that deficits in executive functioning (EF), especially when assessed using rating scales, find that SCT has little association with such deficits while ADHD has strong associations to the extent that ADHD and EF deficits are collinear or the same constructs (Barkley, 2012a, 2012b). Research using neuropsychological tests of EF to compare these two groups have been few in number but even these show some distinctive patterns of deficits between them, though of a far smaller magnitude than do the rating scales of EF (Bauermeister et al., 2012).
In general, these results suggest that SCT children have considerably different patterns of psychiatric comorbidity than ADHD children, being at significantly greater risk for other Disruptive Behavior Disorders, academic placement in programs for behaviorally disturbed children, school suspensions, and receiving psychotherapeutic interventions than are SCT children. The research also appears to indicate that children with SCT symptoms can be distinguished in a number of domains of social adjustment from those with ADHD. Cognitive differences are less consistently noted, but this may have more to do with sample selection procedures in which the SCT children are chosen solely on the DSM inattention list rather than focusing more on symptoms of SCT that are not represented in that list. Based on the evidence available to date, I concur with Milich et al. (2001) that we should begin considering these two conditions as actually separate and unique childhood attention disorders and not as subtypes of an identical attention disturbance such as ADHD.
Two recent surveys ((Barkley, 2012a, 2012b) indicate that SCT is as prevalent as ADHD within the U.S. childhood and adult populations . Whereas ADHD declines to some extent with age, especially across childhood, this is not the case for SCT which arises somewhat later in childhood and remains stable across development (Barkley, 2012a, 2012b). In both children and adults, there is no significant sex difference in SCT symptoms as there is in ADHD, at least in childhood and adolescence.
Many different theories of ADHD have been proposed over the past century to account for the diversity of findings so evident in this disorder. Some of these were discussed above (see “Historical Context”), such as Still’s (1902) notion of defective volitional inhibition and moral regulation of behavior, Douglas’s (1972, 1983) theory of deficient attention, inhibition, arousal, and preference for immediate reward, and the attempts to view ADHD as a deficit in sensitivity to reinforcement (Haenlein & Caul, 1987) or rule-governed behavior (Barkley, 1981, 1989a). Quay (1997), relying on Gray’s neuropsychological model of anxiety (Gray, 1982), proposed that ADHD represented a deficit in the brain’s behavioral inhibition system (BIS). Quay’s hypothesis resulted in increased research on inhibitory and activation (reinforcement) processes in both ADHD (Fischer et al., 2002; Milich et al., 1994) and conduct disorder. Relying on Logan’s “race” model of inhibition, Schachar, Tannock, and Logan (1993) also argued for a central deficit in inhibitory processes in those with ADHD. In this model, an event or stimulus is hypothesized to trigger both an activating or primary response and an inhibitory response creating a competition or race between the two as to which will be executed first. Disinhibited individuals, such as those with ADHD, are viewed as having slower initiation of inhibitory processes relative to normal children.
There is little doubt that poor behavioral inhibition plays a central role in ADHD (see Barkley, 1997b; Nigg, 2001 for reviews). Although important in the progress of our understanding of ADHD, this conclusion still leaves at least two important questions regarding the nature of ADHD unresolved: (1) How does this account for the numerous other associated symptoms and cognitive deficits found in ADHD (described above) and apparently subsumed under the concepts of motor control and executive functioning? (2) How does this account for the involvement of the separate problem with inattention (poor sustained attention) in the disorder? A theoretical model of ADHD developed by the author not only encompasses many of these earlier explanations but may hold the answers to these questions as well as some unexpected directions that future research on ADHD might wish to pursue (Barkley, 1994, 1997a, 1997b, 2001b). The model has been subsequently revised (Barkley, 2012d) to show how deficits in EF can radiate outward to influence the extended phenotype of the individual into several hierarchically arranged levels of increasingly complex adaptive and social functioning.
The original model of EF (and so of ADHD) set forth below and in Figure 1.2 placed behavioral inhibition at a central point in its relation to four other executive functions dependent upon it for their own effective execution. These four executive functions provide for self-regulation, bringing behavior progressively more under the control of time and the influence of conjectured future events over immediate ones and their consequences. The interaction of these executive functions permits far more effective adaptive functioning toward the social future (social self-sufficiency).
Figure 1.2 Diagram illustrating the complete hybrid model of executive functions (boxes) and the relationship of these four functions to the Behavioral Inhibition and Motor Control Systems. From R. A. Barkley (1997). ADHD and the nature of self-control. New York: Guilford. Copyright by Guilford Publications. Reprinted with permission.
Several assumptions are important in understanding the initial model as it is applied to ADHD: (1) The capacity for behavioral inhibition begins to emerge first in development, ahead of most or all these four executive functions but possibly in conjunction with the first, nonverbal working memory. (2) These executive functions emerge at different times in development, may have different developmental trajectories, and are interactive. (3) The impairment that ADHD creates in these executive functions is secondary to the primary deficit it creates in behavioral inhibition (improve the inhibition and these executive functions should likewise improve). (4) The deficit in behavioral inhibition arises principally from genetic and neurodevelopmental origins, rather than purely social ones, although its expression is certainly influenced by social factors over development. (5) The secondary deficits in self-regulation created by the primary deficiency in inhibition feed back to contribute further to poor behavioral inhibition given that self-regulation contributes to the enhancement of self-restraint (inhibition). Finally, (6) the model does not apply to those having SCT. The model has been derived from earlier theories on the evolution of human language (Bronowski, 1977), the internalization of speech (Vygotsky, 1966) and the functions of the prefrontal cortex (Fuster, 1997). The evidence for the original model and its application to ADHD were reviewed in the initial text (Barkley, 1997b).
“Behavioral inhibition” is viewed as being comprised of two related processes: (1) the capacity to inhibit prepotent responses, either prior to or once initiated, creating a delay in the response to an event (response inhibition); and (2) the protection of this delay, the self-directed actions occurring within it, and the goal-directed behaviors they create from interference by competing events and their prepotent responses (interference control). “Prepotent responses” are defined as those for which immediate reinforcement is available for their performance or for which there is a strong history of reinforcement in this context. Through the postponement of the prepotent response and the creation of this protected period of delay, the occasion is set for four other executive functions to act effectively in modifying the individual’s eventual response(s) to the event. This is done to achieve a net maximization of temporally distant consequences rather than immediate consequences alone for the individual. The self-regulation is also protected from interference during its performance by a related form of inhibition (interference control).
The four executive functions are believed to develop via a common process. All represent private, covert forms of behavior that at one time in early child development (and in human evolution) were entirely publicly observable and were directed toward others and the external world at large. With maturation, this outer-directed behavior becomes turned on the self as a means to control one’s own behavior. Such self-directed behaving then becomes increasingly less observable to others as the suppression of the public, peripheral musculo-skeletal aspects of the behavior progresses. The child is increasingly able to act toward themselves without publicly displaying the actual behavior being activated. This progressively greater capacity to suppress the publicly observable aspects of behavior is what is meant here by the terms “covert, privatized, or internalized.” The child comes to be capable of behaving internally (in their brain) without showing that response through their peripheral muscles, at least not to the extent that it is visible to others. As I have discussed elsewhere (Barkley, 1997b, 2001c), this behavior-to-the-self can still be detected in very subtle, vestigial forms as slight shifts in muscle potential at those peripheral sites involving the muscles used in performing the public form of that behavior (e.g., when one engages in verbal thought, one still slightly moves their lips, tongue, larynx, etc.). In this sense, all of the executive functions follow the same general sequence as the internalization of speech (Diaz & Berk, 1992; Vygotsky, 1978, 1987), which in this model forms the second executive function.
Each executive function is hypothesized to contribute to the following developmental shifts in the sources of control over human behavior:
I have elsewhere asserted that the executive functions likely evolved in successive stages in our hominid ancestry from intra-species competition for resources and reproduction in our group living species. The sequence may resemble, to some extent, the same sequential development evident in children today. The first executive function (sensory-motor action to the self, especially visual imagery) begins its development so early in infancy that it must have been crucial to human survival. It may have evolved for the adaptive purposes of reciprocal altruism (social exchange) and generalized vicarious learning. These activities seem to be essential for the survival of our group living species, contributing to reciprocity, cooperation, coalition formation (friendships), the construction of social hierarchies from these coalitions, and pedagogy (Barkley, 2001c, 2012d). Vicarious learning can be considered a form of behavioral plagiarism that, once having arisen in a species, would have set up strong selection pressure for the privatization of one’s behavior, particularly during learning, rehearsal, and other forms of practice, so as not to have one’s behavioral innovations readily appropriated by others (competitors). Other adaptive purposes that may have been served by this and the other three executive functions that develop later are verbal self-instruction, verbal self-defense against social manipulation by others, and self-innovation during social competition. Such evolutionary speculations permit this theory to hypothesize various social deficits that should be evident in ADHD given the executive deficits associated with it that can be tested in subsequent experiments. As is evident below, children with ADHD experience serious difficulties in their social relationships, some of which may arise from the deficits in executive functioning that interfere with reciprocal exchange, vicarious learning, social coalition formation, social self-defense, and self-innovation (improvement).
During the delay in responding created by inhibition, humans activate and retain a mental representation of events in mind (Bronowski, 1977), typically using visual imagery and private audition. The capacity for imagery may allow even infants to successfully perform delayed response tasks to a limited degree (Diamond, 1990; Diamond, Cruttenden, & Niederman, 1994; Goldman-Rakic, 1987). As this capacity increases developmentally, it forms the basis for nonverbal working memory, which has been defined as the ability to maintain mental information on-line so as to guide a later motor response. This activation of past images for the sake of preparing a current response is known as “hindsight” or the “retrospective function” of working memory (Bronowski, 1977; Fuster, 1997). It allows for the retention of events in a temporal sequence that contributes to the “subjective estimation of time” (Michon, 1985). Such temporal sequences can be analyzed for recurring patterns and those patterns can then be used to conjecture hypothetical future events. Anticipating these hypothetical futures gives rise to a preparation to act, or “anticipatory set” (Fuster, 1997). This extension of hindsight forward into time also underlies “forethought” or the “prospective function” of working memory (Bronowski, 1977; Fuster, 1997). And from this sense of future likely emerges the progressively greater valuation of future consequences over immediate ones that takes place throughout child development and early adult life (Green, Fry, & Meyerson, 1994).
Important in this model for understanding the linkage of inattention to disinhibition in ADHD is the critical role played by working memory in maintaining on line (in mind) ones’ intentions to act (“plans”) so as to guide the construction and execution of complex goal-directed actions over time (Fuster, 1997). Such sustained chains of goal-directed actions create persistence of responding giving rise to the capacity of humans to sustain attention (responding) for dramatically long periods of time in pursuit of future goals. As James so eloquently described it: “The essential achievement of the will, in short, when it is most ‘voluntary,’ is to ATTEND to a difficult object and hold it fast before the mind” (p. 815); and, “Everywhere then the function of the effort [voluntary or free will] is the same: to keep affirming and adopting a thought which, if left to itself, would slip away” (p. 818). Thus, self-regulation relative to time arises as a consequence of inhibition acting in conjunction with nonverbal working memory (imagined future goals or states. And since language is used, in part, to express cognitive content, such references to time, sense of past, and sense of future in verbal interactions with others should become increasingly frequent throughout a child's development as his or her sense of time develops.
As extrapolated to those with ADHD, the model predicts that deficits in behavioral inhibition lead to deficiencies in nonverbal working memory and thus: (1) particular forms of forgetfulness (forgetting to do things at certain critical points in time); (2) impaired ability to organize and execute their actions relative to time (e.g., time management); (3) reduced hindsight and forethought; all leading to a reduction in the creation of anticipatory action toward future events. Consequently, the capacity for the cross-temporal organization of behavior in those with ADHD is diminished, disrupting the ability to string together complex chains of actions directed, over time, to a future goal. The greater the degree to which time separates the components of the behavioral contingency (event, response, consequence), the more difficult the task will prove for those with ADHD who cannot bind the contingency together across time so as to use it to govern their behavior as well as others.
Research demonstrates some of these deficits in those with ADHD, such as nonverbal working memory, timing, and forethought (Barkley, 1997b; Barkley, Edwards, et al., 2001; Barkley, Murphy, et al., 2001; Barkley et al., 2008; Murphy et al., 2001; Frazier et al., 2004; Hervey et al., 2004).
One of the more fascinating developmental processes witnessed in children is the progressive internalization or privatization of speech (Diaz & Berk, 1992). During the early preschool years, speech, once developed, is initially employed for communication with others. By 3 to 5-years-old, language comes to be turned on the self. Such overt self-speech is readily observable in preschool and early school age children. By 5 to 7-years-old, this speech becomes somewhat quieter, more telegraphic, and shifts from being more descriptive to being more instructive. Language is now a means of reflection (self-directed description) as well as a means for controlling one’s own behavior. Self-directed speech progresses from being public, to being subvocal, to finally being private, all over the course of perhaps 6 to 10-years-old, thereby giving rise to verbal thought (Diaz & Berk, 1992; Kopp, 1982; Vygotsky, 1987). I have conjectured (Barkley, 1997b) that this internalization of speech represents a larger process in that various other forms of behavior may also be internalized as well (sensory-motor action, emotion, and play).
For those with ADHD, the privatization of speech should be delayed, resulting in greater public speech (excessive talking), less verbal reflection before acting, less organized and rule-oriented self-speech, a diminished influence of self-directed speech in controlling one’s own behavior, and difficulties following the rules and instructions given by others (Barkley, 1997b). Substantial evidence has accumulated to support this prediction of delayed internalization of speech (Berk & Potts, 1991; Landau, Berk, & Mangione, 1996; Winsler, 1998; Winsler et al., 2000). Given that such private self-speech is a major basis for verbal working memory (Baddeley, 2001), this domain of cognitive activity should be impaired in ADHD as well. Evidence suggests this is so, with ADHD children having difficulties with tasks such as digit span backwards, mental arithmetic, paced auditory serial addition, paired associated learning, and other tasks believed to reflect verbal working memory (Barkley, 1997b; Chang et al., 1999; Grodzinsky & Diamond, 1994; Kuntsi et al., 2001). Children with learning disabilities (LD) may also have difficulties with some of these tasks making it unclear to what extent the deficits seen in working memory in ADHD are a function of the overlap of LD with this disorder (Cohen, Vallance, Barwick, Im, Menna, Horodezky, & Isaacson, 2000; Willcutt, et al., 2001). ADHD may impair the actual internalization of speech while LD (reading disorders) may reflect a normal internalization but of an impaired language ability.
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 but that the behavioral reaction to or expression of that emotion is delayed along with any motor behavior associated with it. The delay in responding with this primary emotion, or at least its voluntary components, allows the child time to engage in self-directed behavior that will modify both the eventual response to the event as well as the emotional reaction that may accompany it. This permits a moderating effect both on the primary emotion being experienced subjectively by the child as well as on their eventual public expression of emotional behavior (Barkley, 2010; Keenan, 2000). But it is not just affect that is being managed by the development of self-regulation but the underlying components of emotion as well, these being motivation (drive states) and arousal (Fuster, 1997; Lang, 1995). This internalization and self-regulation of motivation permits the child to induce drive states that may be required for the initiation and maintenance of goal-directed, future-oriented behavior thereby permitting greater persistence toward tasks and activities that may offer little immediate reinforcement but for which there may be substantial delayed reinforcement.
Extending this model to ADHD leads to the following predictions. Those with ADHD should display: (1) greater emotional expression in their reactions to events; (2) less objectivity in the selection of a response to an event; (3) diminished social perspective taking as the child does not delay his or her initial emotional reaction long enough to take the view of others and their own needs into account; and (4) diminished ability to induce drive and motivational states in themselves in the service of goal-directed behavior. Those with ADHD remain more dependent upon the environmental contingencies within a situation or task to determine their motivation than do others (Barkley, 1997b). Research clearly shows that those with ADHD do have significant problems with emotion regulation (Barkley, 2010; Braaten & Rosen, 2000; Maedgen & Carlson, 2000) and that this may be particularly so in that subset having comorbid oppositional defiant disorder (Melnick & Hinshaw, 2000).
The use of private visual imagery as well as private language so as to mentally represent objects, actions, and their properties provides a means by which the world can be taken apart and recombined cognitively rather than physically. The delay in responding allows time for events to be held in mind and then disassembled so as to extract more information about the event before preparing a response to it. Internal imagery and speech permit analysis (taking apart) and out of this process comes its complement-synthesis (recombinations). Just as the parts of speech can be recombined to form new sentences, the parts of the world represented in speech and imagery are, likewise, recombined to create entirely new ideas about the world and entirely new responses to that world (Bronowski, 1977). The world is seen as having parts rather than inviolate wholes – parts capable of multiple, novel recombinations. This permits humans a far greater capacity for creativity and problem solving than is evident in our closest primate relatives. I believe this process results from the internalization of play. Just as speech goes from being overt to self-directed and then covert, so does manipulative and verbal play. This process of mental play, or reconstitution, is evident in everyday speech in its fluency and generativity (diversity) yet it is also evident in nonverbal expression as well, such as in motor and design fluency. The need for reconstitution becomes obvious when obstacles must be surmounted to accomplish a goal. In a sense, reconstitution provides for planning and problem solving to overcome obstacles and attain goals. This mental module produces rapid, efficient, and often novel combinations of speech or action into entirely new messages or behavioral sequences and so gives rise to behavioral innovation.
As applied to ADHD, the model predicts a diminished use of analysis and synthesis in the formation of both verbal and nonverbal responses to events. The capacity to mentally visualize, manipulate, and then generate multiple plans of action (options) in the service of goal-directed behavior and to select from among them those with the greatest likelihood of succeeding should, therefore, be reduced. This impairment in reconstitution will be evident in everyday verbal fluency when the person with ADHD is required by a task or situation to assemble rapidly, accurately, and efficiently the parts of speech into messages (sentences) so as to accomplish the goal or requirements of the task. It will also be evident in tasks where visual information must be held in mind and manipulated to generate diverse scenarios to help solve problems (Barkley, 1997b). Evidence for a deficiency in verbal and nonverbal fluency, planning, problem-solving, and strategy development more generally in children and adults with ADHD is limited, but what exists is consistent with the theory (Barkley, 1997b; Barkley et al., 2008; Frazier et al., 2004; Clark et al., 2000; Hervey et al., 2004; Klorman et al., 1999; Nigg et al., 1998; Oosterlaan et al., 2002).
If the deficit in behavioral inhibition proposed in the current model is housed within the brain’s motor or output system, then its effects should also be evident in the planning and execution of motor actions. Complex fine and gross motor actions require inhibition to preclude the initiation of movements located in neural zones adjacent to those being activated. Inhibition provides an increasing “functional pruning” of the motor system such that only those actions required to accomplish the task are initiated by the individual. Lengthy, complex, and novel chains of goal-directed behavior can be constructed and protected from interference until they have been completed. The model stipulates that those with ADHD should display greater difficulties with the development of motor coordination and especially in the planning and execution of complex, lengthy, and novel chains of goal-directed responses. There is substantial evidence already available for problems in motor development and motor execution in those with ADHD (see Barkley, 1997b, 2006; Harvey & Reid, 1997; Kadesjo & Gillberg, 1999). It remains to be determined whether those with ADHD have more difficulties in producing, executing, and sustaining lengthy and complex chains of novel responses toward goals.
I initially theorized that this executive system may have evolved to support the social activities of reciprocal exchange and cooperation (acting in unison with others for common goals), imitation and vicarious learning, self-sufficiency and innovation, and social self-defense (Barkley, 2001b,2012d), implying that these larger, universally important domains of social development may be impaired by ADHD as well. If so, then deficits in adaptive functioning (self-sufficiency) and other domains of social functioning more generally would be evident in ADHD (as well as other disorders having prefrontal lobe origins), as seems to be the case (Barkley, Shelton, et al., 2002; Roizen, Blondis, Irwin, & Stein, 1994; Shelton et al., 1998; Stein, Szumowski, Blondis, & Roizen, 1995).
In the most recent expansion of this theory of EF (Barkley, 2012d), it has been amended in several respects. First, I have separated out self-awareness from the nonverbal working memory system (sensing to the self) and specified its co-development with inhibition. Self-awareness reflects the direction of the attention systems back on the self, achieving self-monitoring of one’s internal and external states and actions. It is through this self-awareness of one’s present condition and actions that one can then juxtapose it against a visualization of a future state (using nonverbal working memory) and so begin the process of both creating and motivating future-directed or goal-directed actions. Second, I have borrowed the concept of an extended phenotype from the modern literature on evolution to consider how EF produces effects at a considerable distance from the individual that can feed back to influence one’s survival and long-term welfare. Such effects are seen to radiate outward through several levels of a hierarchy of social functioning, with each new level requiring a more extended time horizon across which one is contemplating future goals and the actions needed to attain them. Level I in this model reflects non-executive mental functioning as may be seen in more automatic forms of human behavior and in most nonhuman animals. Level II is the Instrumental-Self-Directed one achieved when humans develop self-directed actions that they are using for self-regulation. This is the beginning of executive functioning. Level III is the initial outward extension of these mental functions into the realm of day-to-day behavior and survival, labeled as Methodical-Self-Reliant. It is here that one is using executive functioning for self-care, social independence or self-reliance, and social self-defense against being manipulated by others against one’s welfare. Achievement of this level leads, in combination with a further expansion of foresight, into Level IV, which is the Tactical-Reciprocal level of social functioning. Here the individual is using EF not just for self-sufficiency but for selectively interacting with others in social exchange or reciprocity in which goods and services are exchanged with others to the benefit of both parties rather than the parasitic relationship in which one takes advantage of another with there being no mutual benefit to the interaction. This results in the development of social networks among self-interested reciprocators, such as friendships, that also provide the basis for economic exchange and other forms of economic functioning. After awhile, this level can lead up to the final level of EF in social functioning which is the development of social cooperatives. Here individual reciprocators join together to act in unison to achieve goals that one cannot attain acting alone or through simple reciprocity. This expansion of the initial model into these zones of social functioning illustrates the crucial importance of EF to effective social functioning to see to one’s longer term survival and welfare. It also demonstrates the extended phenotypic effects of the EF system into domains of functioning such as peer friendships, education, occupational functioning, economic activities, and even legal and governmental activities. Impairment to the EF system will cause a contraction or collapsing of these levels of social functioning.
The present model of EF, as extended to understanding ADHD, shows how the findings noted above under “Associated Cognitive Impairments” can now be integrated into a more unifying theory of the disorder. ADHD is a pervasive disorder across all of the initial EFs and thus causes a pervasive impact on these various extended phenotypic levels of social functioning. Undoubtedly, this theory is imperfect, requiring a great deal of research to clarify the nature of each component in the model, to evaluate the strength of the relationship of each component to behavioral inhibition and to the other components, to elucidate the developmental progression of each component and their ordering, and to critically test some of the previously unexpected predictions of the model as applied to ADHD (i.e., diminished time management, reduced references to time in verbal interactions, the impact of ADHD on analysis/synthesis and self-innovation, etc.).
All useful theories are imperfect and time-limited. What we ask of them is not perfection from birth, but the more pragmatic standard of greater utility than previously existing models or theories. Competing theories of ADHD have limited themselves to just elucidating the nature of the inhibitory deficit (Quay, 1997; Sonuga-Barke et al., 1994) or of a deficient energetic pool (Sergeant, 2005), while ignoring the associated cognitive, emotional, and social deficiencies associated with it and explaining why they exist. The present theory offers more utility in that it addresses the origins of those associated problems, is more testable and hence falsifiable, provides a better link to normal human development, and yields a greater understanding of the basis for managing the disorder than do other extant models. Regardless of what theory may replace it in the future, it will likewise have to deal with the evidence which points to problems with inhibition, self-awareness, and these four executive functions and their extended phenotypic effects into the surrounding levels of social functioning (self-reliance, reciprocity, and cooperation).
This appreciation of the linkage among the executive functions in the model, the self-regulation they permit, and the goal-directed persistence that derives from self-control explain several important findings about the link between disinhibition (hyperactive-impulsive behavior) and inattention. It is possible to see, now, why the problems with hyperactive-impulsive behavior arise first in the development of ADHD to be followed within a few years by the problems with inattention. And it also explains the nature of that inattention as it arises. The inattention reflects a deficit in executive functioning, especially working memory, and so is really a form of intention deficit (attention to the future).
There are numerous implications for the clinical treatment or management of ADHD that stem from the model of executive functions and self-regulation developed here and extrapolated to ADHD (see Barkley, 1997b, 2006, 2012d). Space here permits a brief discussion of only the more important or obvious ones.
The totality of the deficits associated with ADHD serve to cleave thought from action, knowledge from performance, past and future from the moment, and the dimension of time from the rest of the three-dimensional world more generally. This definition means that ADHD is not a disorder of knowing what to do but of doing what one knows. It produces a disorder of applied intelligence by partially dissociating the crystallized intelligence of prior knowledge from its application in the day-to-day stream of adaptive functioning. ADHD, then, is a disorder of performance more than a disorder of skill—a disability in the “when” and “where” and less in the “how” or “what” of behavior. Those with ADHD often know what they should do or should have done before, but knowing provides little consolation to them, little influence over their behavior, and often much irritation to others. Such knowledge seems to matter little when they are actually behaving at particular moments.
Events predicted to lie ahead in the distant future will elicit planning and anticipatory behaviors in others at a far greater future time horizon than is likely to be seen in those with ADHD. Those with ADHD, instead, may not begin to make preparations, if at all, until the event is far closer in time, imminent, or even immediately upon them. This pattern is a recipe for a life of chaos and crisis. Individuals with ADHD squander their energies dealing with the emergencies or urgencies of the more temporal now when a few moments forethought and planning could have eased the burden and likely avoided the crisis. ADHD greatly constricts the temporal window or time horizon over which those with the disorder consider the consequences of their actions, and it is through no fault of their own that they find themselves in this predicament.
I fully appreciate the conundrum such conclusions about ADHD pose for the notion of personal accountability and responsibility within society. The argument here could be used by some to seek a finding of “diminished capacity” in the mental status of those with ADHD, as that capacity was originally conceived to be in common law. That capacity was the power to consider one’s actions in light of past experience and future consequences; to deliberate the outcomes of one’s acts relative to time. In a way, those seeking to make such a case would be correct in this analysis – ADHD does create a diminished capacity to deliberate on the outcomes of one’s actions.
It is clear that ADHD is disrupting the cross-temporal organization of behavior, loosening the binding of past and future consequences to the deliberations on current behavior, and lessening the capacity to bridge delays among the elements of a behavioral contingency. Given this circumstance, I submit that the required response of others to the poor self-control shown by those with ADHD, then, is not to eliminate the outcomes of their actions and to excuse them from personal accountability. It is to temporally tighten up those consequences, emphasizing more immediate accountability. Consequences must be made more immediate, increased in their frequency, made more “external” and salient, and provided more consistently than is likely to be the case for the natural consequences associated with one’s conduct. More feedback, more often is the resulting conclusion; more accountability and holding to responsibility, not less, are the watchwords in helping those with ADHD. Their problem is not so much being held accountable for the outcomes of their actions but the delays in that accountability that are often inherent in those natural outcomes. The most salient natural outcomes of our behavior are often those that are delayed in time, such as eventually being retained in grade after several years of poor school performance, being suspended from school after years of repeated misconduct in that environment, and being arrested and jailed for years of impulsive criminal conduct. The provision of more proximal outcomes more often should preclude or minimize the likelihood of these more harmful, socially damaging, yet temporally distal natural outcomes of the conduct of those with ADHD.
ADHD is, therefore, not an excuse but an explanation, not a reason to dismiss outright the ultimate consequences of one’s actions but a reason to increase accountability by making it more temporally contiguous with those actions. Time, not consequences, is the problem in life’s behavioral contingencies for those with ADHD. Therefore, removing time, not removing outcomes, is the solution to their problem of “diminished capacity.” Time and the future are the nemeses of those with ADHD, not outcomes and personal responsibility. And it is through no fault of their own that they find themselves in this temporal dilemma. Thus, society should not absolve those with ADHD of accountability or responsibility for their actions, but it should absolve them of the moral indignation of others that often accompanies this issue.
This text takes as its premise that time is the ultimate yet nearly invisible disability afflicting those with ADHD. If one cannot see spatial distances very well, the solution is corrective lenses. If one neglects to respond to events at visuospatial distances as a consequence of brain injury, the prescription is cognitive rehabilitation. But what are the solutions to those with a myopia or blindness to time and a neglect of distances that lie ahead in time? And how can those individuals be expected to benefit from any corrective or rehabilitative treatments when the very cognitive mechanisms that subserve the use of these treatments – the selfregulatory or executive functions—are precisely where the damage caused by ADHD lies?
Teaching time awareness and management to a person who cannot perform time awareness or time management, no matter how much they may know about time and time management, is not going to prove especially fruitful. Given the information in this section, we should not be surprised to find that the person with ADHD often may not even show up for the appointments for such rehabilitation or show up on time given his or her disability in performing within time. Understanding time and how one comes to organize behavior within it and toward it, then, is a major key to the mystery of understanding ADHD.
An important implication of this model is that the most useful treatments are those in place in natural settings at the point of performance, where the desired behavior is to occur. Ingersoll and Goldstein (1993) say that this “point of performance” seems to be a key concept in the management of those with ADHD. The further away in space and time the location of the intervention from this point of performance is, the less effective it should prove to be for managing or treating those having ADHD. This implication immediately suggests that clinic-delivered treatments, such as play therapy, counseling of the child, neurofeedback, or other such therapies, are not as likely to produce clinically significant improvement in ADHD, if at all, in comparison to treatments undertaken by caregivers in natural settings at the places and times the performance of the desired behavior is to occur. The latter treatments would be programs such as behavior modification that undertake to restructure the natural setting and its contingencies to achieve a change in the desired behavior and to maintain that desired behavior over time.
This perspective suggests an additional implication of the model for treating those with ADHD: Any such treatment will be purely symptomatic. That is, treatments that alter the natural environment to increase desired behavior at critical points of performance will result in changes in that behavior and its maintenance over time only insofar as the treatments are maintained in those places over time. Behavioral treatments or any other such method of management applied at the point of performance is not altering the underlying neuropsychological and largely genetic deficits in behavioral inhibition. It only provides immediate relief from these deficits by reducing or restructuring those environmental factors that appear to handicap the performance of the individual with ADHD in that setting. Eliminate the behavioral treatments and environmental structure created to sustain the behavior and, to a large degree, a reversal of the treatment effects should occur.
Behavior modification treatments may be highly successful in altering behavior in the contexts in which they are applied and in sustaining those treatment gains as long as they are applied. But the removal of the contingencies often spells the death knell for further maintenance of these treatment gains. Nor should we expect to find that such treatments, even when in place, produce generalization of treatment effects to other settings where no such treatments are in place. Thus, treatment of the individual with ADHD is not so much a “cure” that eliminates the underlying cause of the disorder. It is, instead, a means of providing temporary improvement in the symptoms of the disorder, and even then only in those settings in which such treatments are applied. Although this treatment may be initiated to reduce those future risks that are secondary consequences of having unmanaged ADHD, as yet, little or no evidence suggests that such benefits accrue from these short-term treatments unless they are sustained over the long term. Nevertheless, the management of behavior in the immediate environments in which it is problematic for those with ADHD is a laudable goal in and of itself, even if it is not shown to produce additional benefits for the individual in later years. After all, the reduction of immediate distress and improvement in immediate success is a legitimate treatment outcome for improving the immediate quality of life for the individual.
This theory suggests a more specific implication for the management of ADHD. Only a treatment that can result in improvement or normalization of the underlying neuropsychological deficit in behavioral inhibition is likely to result in an improvement or normalization of the executive functions dependent on such inhibition. To date, the only treatments that exist that have any hope of achieving this end are the ADHD medications or other psychopharmacological agents that improve or normalize the neural substrates in the prefrontal regions that likely underlie this disorder. Evidence to date suggests that this improvement or normalization in inhibition and some of the executive functions may occur as a temporary consequence of active treatment with stimulant medication, yet only during the time course the medication remains within the brain. Research shows that clinical improvement in behavior occurs in as many as 75% to 92% of those with the hyperactive-impulsive form of ADHD and results in normalization of behavior in approximately 50% to 60% of these cases, on average. The model of ADHD developed here, then, implies that ADHD medications are not only a useful treatment approach for the management of ADHD but the predominant treatment approach among those treatments currently available because it is the only treatment known to date to produce such improvement/normalization rates.
Society may view medication treatment of ADHD children as anathema largely as a result of a misunderstanding of both the nature of ADHD specifically and the nature of self-control more generally. In both instances, many in society wrongly believe the causes of both ADHD and poor self-control to be chiefly social in nature, with poor upbringing and child management by the parents of the poorly self-controlled child seen as the most likely culprit. The present model states that not only is this view of ADHD incorrect but so is this view of self-regulation. And this model also implies that using stimulant medication to help to temporarily improve or alleviate the underlying neuropsychological dysfunction is a commendable, ethically and professionally responsible, and humane way of proceeding with treatment for those with ADHD.
Turning to more specific implications of this model of ADHD for treatment, it can be reasoned that if ADHD results in an under control of behavior by internally represented forms of information, caregivers should get that information “externalized” as much as possible, whenever feasible. These internal forms of information, if they have been generated at all, appear to be extraordinarily weak in their ability to control and sustain behavior in its more futuristic and beneficial form for the individual with ADHD. Self-directed visual imagery, audition, and the other covert resensing activities that form nonverbal working memory as well as covert self-speech, if they are functional at all at certain times and contexts, are not yielding up information of sufficient power to control behavior. That behavior is remaining largely under the control of the salient aspects of the immediate three-dimensional context. The solution to this problem is not to carp at ADHD individuals to simply try harder or to remember what they are supposed to be working on or toward. It is instead to take charge of that immediate context and fill it with forms of stimuli comparable to their internal counterparts that are proving so ineffective. In a sense, clinicians treating those with ADHD must beat the environment at its own game. Sources of high-appealing distracters that may serve to subvert, pervert, or disrupt task-directed behavior should be minimized whenever possible. In their place should be forms of stimuli and information that are just as salient and appealing yet are directly associated with or an inherent part of the task to be accomplished.
Specifically, parents or educators of children with ADHD may need to rely on external prompts, cues, reminders, or even physical props that supplement the internal forms of information that are proving ineffective. If the rules that are understood to be operative during classroom individual deskwork, for instance, do not seem to be controlling the ADHD child’s behavior, they should be externalized. The rules can be externalized by posting signs about the classroom that are related to these rules, or by creating a poster displayed at the front of the class or typed on a card taped to the child’s desk that reminds the child of these rules. Having the child verbally self-state these rules aloud before and during these individual work performances may also be helpful. Recorded reminders on a digital recorder, which the child listens to through an earphone while working is another way to externalize the rules and put them at the points of performance. It is not the intention of this course to articulate the details of the many treatments that can be designed from this model. All I wish to do here is simply show that with the knowledge this model provides and a little ingenuity, many of these forms of internally represented information can be externalized for better management of the child or adult with ADHD.
Chief among these internally represented forms of information that either need to be externalized or removed entirely from the task are those related to time. As I have stated earlier, time and the future are the enemies of people with ADHD when it comes to task accomplishment or performance toward a goal. An obvious solution, then, is to reduce or eliminate these elements of a task when feasible. For instance, rather than assign a behavioral contingency that has large temporal gaps among its elements to someone with ADHD, those temporal gaps should be reduced whenever possible. In other words, the elements should be made more contiguous.
For example, let us consider a book report assigned to an ADHD student. That report is assigned today but stipulates that the report is due in two weeks, after which it will be at least one week or more before the grade for it is returned to the student. There is a two-week gap between the event (assignment) and response (report) in this contingency as well as a one-week gap between the response and its consequence (the grade). Moreover, the grade is a rather weak source of motivation for someone with ADHD as it is symbolic, secondary, and a formative type of augmental in rule-governed behavior. This additional implication of the model, dealing with the requirement for more external sources of behavioral motivation to undergird task or goal-directed performances for those with ADHD, is discussed later. The important point here is that large gaps in time exist within this temporal contingency that are detrimental to the successful performance of this contingency by those with ADHD. This model suggests, instead, that instructions for the task be presented to the child with ADHD as follows: (1) Read five pages right now from your book, then (2) write two to three sentences based on what you read, after which (3) I will give you five tokens (or some other immediate privilege) that you have earned for following this rule. Although the example may seem simplistic, the concepts underlying it are not; those concepts are critical to developing effective management programs for those with ADHD according to this model. Gaps in time within behavioral contingencies must be reduced or eliminated whenever possible.
When they cannot be eliminated, the sense of time itself, or its passage, needs to be externalized in some way. If the individual’s internal, cognitive clock is not working well, an external clock in the immediate context should become part of the task’s performance. For instance, instead of telling a child with ADHD that he or she has 30 minutes to get some classwork or school homework or a chore done, caregivers should consider other, more helpful options. Not only does the rule of the assignment need to be more externalized, for example, by using printed rules on chore, homework, or classwork cards, discussed previously, but the time interval itself should be as well. Caregivers can accomplish this goal by writing that number on the card to signify the time limit and also by setting a spring-loaded kitchen cooking timer to 30 minutes and placing it before the child while he or she performs the task. Then there is little need for the child to fall back on an internal sense of this temporal duration, inaccurate as I have shown that is likely to be. Time can be externalized within tasks or settings in many ways that might prove beneficial to those with ADHD and simply require some cleverness to construct. Likewise, other ways of “bridging” temporal delays may help those with ADHD – limited only by the creativity of the clinician or caregiver. The point I wish to emphasize here, once again, is not the method but the concept – externalize time and the bridges we use across it!
Yet there is a major caveat to all of these implications for externalizing forms of internally represented information. This caveat stems from the component of the model that deals with self-regulation of emotion, motivation, and arousal: No matter how much clinicians, educators, and caregivers externalize the internalized forms of information by which they desire the person with ADHD to be guided (stimuli, events, rules, images, sounds, etc.), it is likely to prove only partially successful, and even then only temporarily, if internal sources of motivation are not augmented with more powerful external forms as well. It is not simply the internally represented information that is weak in those with ADHD, it is the internally generated sources of motivation associated with them that are critical to driving goal-directed behavior toward tasks, the future, and the intended outcome in the absence of external motivation in the immediate context. Addressing one form of internalized information without addressing the other is a sure recipe for ineffectual treatment. Anyone wishing to treat or manage those with ADHD has to understand that sources of motivation must also be externalized in those contexts in which tasks are to be performed, rules followed, and goals accomplished. Complaining to ADHD individuals about their lack of motivation (laziness), drive, will power, or self-discipline will not suffice. Pulling back from assisting them to let the natural consequences occur, as if this will teach them a lesson that will correct their behavior, is likewise a recipe for disaster. Instead, artificial means of creating external sources of motivation must be arranged at the point of performance in the context in which the work or behavior is desired.
For example, token systems in the form of artificial reward programs for children five years of age and older are one of the best means to subserve the weak internal sources of motivation in ADHD children. Plastic poker chips can be given throughout and at the end of the work performance, as suggested earlier in the book report example. These chips can be exchanged for access to other more salient privileges, rewards, treats, and so on that the child with ADHD may desire. The point here is not as much the technique as the concepts. Rewards, in most cases artificial or socially arranged ones, must be instituted more immediately and more often throughout a performance context for those with ADHD and must be tied to more salient reinforcers that are available within relatively short periods if the behavior of those with ADHD is to be improved. This point applies as much to mild punishments for inappropriate behavior or poor work performance as it does to rewards. And, as I noted earlier, such artificial sources of motivation must be maintained over long periods or the gains in performance they initially induce will not be sustained.
The methods of behavior modification are particularly well suited to achieving these ends and many techniques exist within this form of treatment that can be applied to those with ADHD. What first needs to be recognized, as this model of ADHD stipulates, is that (1) internalized, self-generated forms of motivation are weak at initiating and sustaining goal directed behavior; (2) externalized sources of motivation, often artificial, must be arranged within the context at the point of performance; and (3) these compensatory, prosthetic forms of motivation must be sustained for long periods.
Concerning the latter recommendation, it is certainly likely that with neurological maturation, those with ADHD improve their ability to self-generate motivation, as is implied in the concept of a developmental delay. They merely lag behind their normal peers in this capacity at each age at which we examine them. Thus, like normal children, we can diminish their reliance on external sources of motivation and the intensity and frequency with which they are arranged as they mature and develop the capacity for self-motivation. This means that behavior modification programs using artificial rewards can be “thinned” or reduced in their frequency and immediacy over time as the ADHD child’s maturation results in an increase in the ability to self-motivate. But this model also argues that at any age at which we work with an individual with ADHD, such external sources of motivation must still be relied on more than is normal for the individual’s age even though with less rigor, immediacy, frequency, and consistency than at earlier ages.
Thus far, I have tried to address the treatment implications for the first three executive function deficits in the model of ADHD created here: working memory, internalized speech, and self-regulated motivation. How to deal with the problem of reconstitution predicted to be deficient in those with ADHD seems to me to be more difficult to address. If more were known about the process of analysis/synthesis and the behavioral creativity to which it gives rise, ways of externalizing this process might be more evident and useful to those with ADHD in this domain of their executive deficits. Perhaps taking the problem assigned to the ADHD individual and placing its parts on some externally represented material would help, along with prompting and guidance as to how to take apart and move about these forms of information to recombine them into more useful forms. Adults seem to do this when struggling with a difficult problem; they make their previous internal forms of problem-solving behavior external. For instance, we see this when people talk to themselves out loud when solving a difficult puzzle or acquisition of a complex procedure; begin to doodle on a pad, playing with certain designs; free associate publicly to the topic of the problem under discussion; or even reduce a number of words to slips of paper or pieces of magnets and then randomly reshuffle them to create new arrangements. (The game Magnetic Poetry does this with words on small magnetic strips, as Boggle, Scrabble, and anagrams do with letters.) Regardless, the point of this discussion is the same as for the other executive functions – by externalizing what should otherwise be internally represented information and even externalizing the process by which that information is being generated caregivers may be able to assist those with ADHD in compensating for their weak executive functions. Again, such structuring of tasks and contexts must be sustained over long periods if the gains it initially achieves are to be sustained as well.
The foregoing leads to a much more general implication of this model of ADHD: The approach taken to its management must be the same as that taken in the management of other chronic medical or psychiatric disabilities. I frequently use diabetes as an analogous condition to ADHD in trying to assist parents and other professionals in grasping this point. At the time of diagnosis, all involved realize that no cure exists as yet for the condition. Still, multiple means can provide symptomatic relief from the deleterious effects of the condition, including taking daily doses of medication and changing settings, tasks, and lifestyles. Immediately following diagnosis, the clinician designs and brings to bear a treatment package on the condition. This package must be maintained over long periods to maintain the symptomatic relief that the treatments initially achieve. Ideally, the treatment package, so maintained, will reduce or eliminate the secondary consequences of leaving the condition unmanaged. However, each patient is different and so is each instance of the chronic condition being treated. As a result, symptom breakthrough and crises are likely to occur periodically over the period of treatment, which may demand reintervention or the design and implementation of entirely new treatment packages. Throughout all this management, the goal of the clinician, family members, and patients themselves is to try to achieve an improvement in the quality of life and success for the individual, though it may never be totally normal.
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