STOP, LOOK, AND LISTEN: The Challenge for Children with ADHD
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Descripción: Attention deficit-hyperactivity disorder (ADHD) is a common neuropsychiatric disorder that appears in 4% t...
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Issues in Comprehensive Pediatric Nursing, 23:1–13, 2000 Copyright ã 2000 Taylor & Francis 0146-0862/00 $12.00 + .00
STOP, LOOK, AND LISTEN: The Challenge for Children with ADHD JULIE B. MEAUX, RNC, MNSC The University of Central Arkansas, Conway, Arkansas, USA
Attention deficit-hyperactivity disorder (ADHD) is a common neuropsychiatric disorder that appears in 4% to 13% of the U. S. population. Contrary to earlier beliefs, ADHD frequently persists into adolescence and adulthood and is associated with poor health choices and risk-taking behavior. Despite a vast amount of scientific literature addressing the disorder, many misconceptions and myths prevail creating confusion for children, their families, and health professionals as they attempt to make treatment decisions. One new theoretical model of ADHD shows promise in its ability to provide a more comprehensive explanation of the disorder; it could prove useful in the development of interventions and research programs to improve health maintenance and decrease health–risk behavior in the ADHD population.
Young children are notorious for the manner in which they dash from one activity to another with robust enthusiasm. High energy and activity levels, short attention spans, and a need for immediate gratification typically characterize their actions. Emotional reactions usually are readily apparent as they impulsively respond to events around them without much forethought or planning. Accountability for controlling one’s impulses increases with age, and by the early school years, children experience increased demands that require sustained attention and self-control. When children continue to display levels of inattention, hyperactivity, and impulsivity that are inappropriate for their age, they experience problems across the social, cognitive, academic, familial, and emotional domains of development. Attention deficit-hyperactivity disorder (ADHD), a common neuropsychiatric disorder, often surfaces during the child’s early school years. The Received 15 August 1999; revised 25 November 1999; accepted 5 December 1999. Address correspondence ot Julie B. Meaux, RNC, Department of Nursing, University of Central Arkansas, 201 Donaghey St., Conway, AR, USA
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hallmark characteristics of ADHD are developmentally inappropriate levels of inattention, hyperactivity, and impulsivity (American Psychiatric Association, 1994). These characteristics are thought to develop early and, contrary to previous beliefs, often persist into adolescence and adulthood (Barkley, 1997b). Longitudinal studies reveal that adolescents with persistent ADHD symptoms, compared with those without such symptoms, are less likely to complete high school and are at increased risk for substance abuse, unintentional injuries, and delinquent and antisocial behavior (Barkley, Fischer, Edelbrock, & Smallish, 1990; Gittelman, Mannuzza, Shenker, & Bonagura, 1985; Satterfield, Hoppe, & Schell, 1982; Weiss, Hechtman, & Perlman, 1978). These health-risk behaviors can lead to serious injuries and even mortality. Current estimates indicate that the prevalence of ADHD is approximately 4% to 6% in the U.S. population (Jaksa, 1998) and may be as high as 13% in U.S. inner cities (Goldman, Genel, Bezman, & Slanetz, 1998). Despite the prevalence of ADHD and the vast amount of scientific literature addressing the disorder, many common misconceptions and myths continue to confront children, their families, and health professionals as they attempt to make treatment decisions. Differing theories on the etiology of ADHD have contributed to the confusion. A review of the history of ADHD from its earliest identification at the beginning of the 20th century reveals common themes that serve as the basis for current conceptualizations of the disorder as well as ideas that have persisted despite the lack of scientific support. HISTORICAL OVERVIEW The earliest scientific reference to children with poor behavioral control is attributed to George Still (Hassler, 1992). Still’s description in 1902 of symptoms of aggressiveness, resistance to discipline, poor self-control, hyperactivity, and poor attention in a group of children from his clinical practice is remarkably consistent with what we now call ADHD. He believed the children exhibited a “defect in moral control” resulting from a biological predisposition or pre- or postnatal injury (Hassler, 1992). As a result of the encephalitis epidemic of 1918, support mounted for the theory that brain damage caused poor behavioral control and hyperactivity (Strecker & Ebaugh, 1924). Children who recovered from acute encephalitis often displayed drastic personality changes, hyperactivity, distractibility, antisocial behavior, and, most notably, a resistance to discipline. Clinicians noted the same cluster of behavioral symptoms in children who suffered from other brain disorders, such as epilepsy, head injury, or anoxia. The apparent etiologic link resulted in labeling the disorder as “minimal brain damage” (Strecker & Ebaugh, 1924).
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Controversy over the etiology of the disorder arose during the 1930s when investigators began to apply different terms to the same cluster of behavioral symptoms (Kahn & Cohen, 1934; Levin, 1938). The label “restlessness” syndrome was applied to a group of children who displayed normal to superior intelligence and had no evidence of brain injury, but they exhibited symptoms of hyperactivity, poor attention span, and impulsivity. Scientists believed their symptoms stemmed from a psychological etiology caused by parental overindulgence or neglect (Levin, 1938). In contrast, Kahn and Cohen (1934) postulated that defective brainstem organization caused “organic driveness,” a term they introduced to describe hyperactivity. The use of stimulant drugs for behavioral problems started in 1937 when Dr. Charles Bradley accidentally discovered that children with hyperactivity had a paradoxical response to the drugs. After taking Benzedrine the children experienced improved school performance, decreased disruptive behavior, and a greater ability to concentrate (Bradley, 1937). Dr. Bradley’s findings stimulated little interest in the scientific community until the early 1960s when clinical trials began to replicate his results. During the 1950s and 1960s, the scientific community began to seriously question the concept of inferred brain damage based on behavioral symptoms. As research surrounding the disorder began to proliferate, focus slowly shifted away from the inference of brain damage to the primary symptom of hyperactivity. Scientists replaced the term “minimal brain damage” with “hyperkinetic syndrome” to describe the broad class of behavior and learning disorders (Aman, 1984; Solomons, 1965; Stewart, 1970). The growing body of literature in the 1970s again caused scientists to shift their focus. The symptoms of poor attention span and problems with impulse control began to receive more attention than the symptoms of hyperactivity (Douglas, 1972). The establishment of diagnostic criteria and an official name change (attention-deficit disorder and later attention-deficit hyperactivity disorder) took place. During this same period, the use of stimulant medications for school-age hyperactive children rapidly increased. Despite the scientific evidence supporting the effectiveness of stimulant medication for these children, public and professional misgivings about “drugging” schoolchildren for behavior problems created a backlash (Barkley, 1976; Schrag & Divoky, 1975). Theories of environmental causes of hyperactivity, such as diet, rapid cultural changes, and poor parenting, received much attention in the public press during the 1970s, but the scientific community found little evidence to support these claims (Barkley, 1998b; Becker, 1974; Block, 1977; Rutter, 1977).
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During the 1980s the focus of research shifted again—and has continued into the 1990s—as a result of a failure to find primary deficits in attention in children with ADHD. Several investigators began to look at motivational factors and reinforcement mechanisms as the core difficulty in ADHD (Barkley, 1981; Quay, 1987). Other researchers started to focus on possible psychophysiological or genetic explanations of the disorder (Biederman et al., 1995; Goodyear & Hynd, 1992; Mariani & Barkley, 1997; Pennington, Groisser, & Welsh, 1993). Unfortunately, the lay media have continued to exploit and exaggerate many of the unsubstantiated theories of the 1970s, creating a disparity between pervasive societal beliefs about ADHD and scientific findings that often contradict them. Despite the plethora of research on ADHD, no one developed a theoretical model that accounts for the impairments frequently associated with the disorder. A newly developed theoretical model of ADHD, based on the collective research of several investigators, shows promise in its ability to provide a more comprehensive explanation of the core symptoms and secondary deficits of ADHD (Barkley, 1997a, 1997b). This hybrid model of executive functions could prove useful in understanding and treating the disorder and focusing future research. HYBRID MODEL OF EXECUTIVE FUNCTIONS Origin of the Model Barkley’s hybrid model of executive functions is a deductive theory, derived primarily from Bronowski’s (1977) theory on the uniqueness of human language, Fuster’s (1997) theory on neuropsychological functions governed by the prefrontal cortex, and the work of Goldman-Rakic (1995). Bronowski (1977) identified four unique properties of human language: prolongation, separation of affect, internalization of language, and reconstitution. He argued that human language is more than a simple means of communication, it is a means of reflection as well. Reflection can only occur if there is a delay between a stimulus and the response to the stimulus, during which humans deliberate and test plans of action. Bronowski attributed the ability to delay responses and the four cognitive functions associated with it to the brain’s prefrontal cortex. Fuster’s theory (1997) of prefrontal functions has much in common with Bronowski’s model. He recognized functions of the prefrontal cortex necessary for cross-temporal organization of behavior. Fuster viewed these executive functions as separate but highly interactive. These executive functions included hindsight, forethought, response inhibition, and interference control. He also proposed that the functions of the prefrontal cortex exert a direct influence on goal-directed motor activity, suggesting
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that poor inhibition and interference control cause distractibility, hyperactivity, and impulsiveness. The work of Goldman-Rakic (1995) has contributed to the knowledge of anatomical and neurophysiological mechanisms of the prefrontal cortex. Her work with primates has led to the understanding that regulation of behavior by mentally represented stimuli rather than simply by external control occurs in the prefrontal cortex. Recent neuroimaging studies in humans have lent support to the idea of separate, yet interactive, executive functions subserved by the prefrontal cortex (McCarthy, Puce, Constable, Krystal, Gore, & Goldman-Rakic, 1996; Smith, Jonides, & Koeppe, 1996). There are several overlapping points in each of these models, particularly the role of the prefrontal cortex and the development of self-regulation. Barkley’s hybrid model builds on earlier work and further defines the role of executive functions in the development of self-regulation and goal-directed behavior (Barkley, 1997b). The three-tiered model contains six components (Figure 1). The first tier of the model consists of the component of behavioral inhibition and forms the foundation for all other components. Behavioral Inhibition Behavioral inhibition is defined as the ability to inhibit a prepotent response, interrupt an ongoing response, and protect a response from internal or external interference or interference control (Barkley, 1998b). A prepotent response always has or has had immediate reinforcement (positive or negative). The individual cannot engage in behavior to maximize future outcomes if he or she already has acted to maximize immediate gratification. The ability to interrupt an ongoing response or response pattern permits a delay that allows the individual to decide whether to continue responding. Flexibility in ongoing behavior allows the individual to change behavior as the context of the situation changes. Behavioral inhibition also involves interference control. This inhibitory process protects overt and covert behavior from internal and external interference and allows for the execution of cognitive functions necessary for selfcontrol (Barkley, 1997b). Executive Functions The second tier of the model contains four executive functions that depend on behavioral inhibition. Behavioral inhibition does not cause the four executive functions to occur, but it merely sets the stage for their performance and protects that performance from interference. The four
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Figure 1. Barkley’s hybrid model of executive functions (boxes) and the relationship of these four functions to the behavioral inhibition and motor control systems. [From Barkley (1997b). Copyright 1997 by The Guilford Press. Reprinted by permission.]
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executive functions are nonverbal working memory, verbal working memory, self-directed affect/motivation/arousal, and reconstitution (Barkley, 1997a, 1997b, 1998a). Nonverbal Working Memory Nonverbal working memory is defined as “covert sensing to the self” (p. 235) and refers to the ability to hold information in the mind after a stimulus is gone (Barkley, 1998a). Covert motor and sensory imagery (sights, sounds, smells, and tastes) provide internally represented information that is used to organize and guide behavior across time toward a goal. Nonverbal working memory allows the individual to covertly reactivate prior experiences to guide behavior. Sense of time, hindsight, forethought, and the ability to imitate or learn from others is contingent on nonverbal working memory. Verbal Working Memory Verbal working memory is defined as the internalization of self-directed speech (Barkley, 1997a). It allows the individual to use covert selfdirected language to process or contemplate the nature of an event or situation before responding. Younger children frequently speak out loud to themselves as they solve problems. They keep a running audible dialogue to remind themselves of what they are doing. After the age of 6, they progressively internalize self-directed speech, and generally by age 10, audible self-directed speech disappears. The internalization of selfdirected speech allows for self-reflection, self-questioning, following rules and instructions, and the development of personal rules (Barkley, 1998a). Self-Regulation of Affect/Motivation/Arousal The third executive function in the model enables people to covertly control emotions, motivate themselves, and control arousal states (Barkley, 1998a). The ability to selectively moderate emotional states and produce self-motivation normally increases across childhood, adolescence, and early adulthood. Moderation of emotional states and self-motivation enables individuals to achieve goals and behave in socially acceptable ways (Barkley, 1997a, 1997b, 1998a). Reconstitution Reconstitution is described as the ability to covertly analyze and synthesize behavior (Barkley, 1998a). Individuals analyze the actions and speech of others by covertly breaking down behavioral sequences and language into individual units. Synthesis allows for combining behaviors and speech into new patterns without having to learn each step or experience every situation. The cognitive function of reconstitution gives individuals flex-
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ibility, creativity, and the ability to have goal-directed behavior (Barkley, 1997a, 1997b, 1998a). Motor Control/Fluency/Syntax The executive functions are covert, self-directed, and internally derived behaviors that contribute to greater control, flexibility, and complexity of goal-driven motor actions. Therefore, motor control occupies the third tier of Barkley’s model because all other components influence it. According to this model, self-control requires that a person recognize factors—cues and consequences—that influence his or her own behavior and employ those factors to produce desired, intentional, and goaldirected behavior. Self-control requires constant self-evaluation and introspection (Barkley, 1997a, 1997b). THE MEANING FOR THE CHILD WITH ADHD The basic precept of the model when applied to ADHD holds that the primary impairment is that of behavioral disinhibition (Figure 2). Based on this model, one can predict that behavioral disinhibition gives rise to secondary deficits in the four executive functions, resulting in behavior that is less internally guided, less purposeful and goal-directed, less governed by and oriented to time, and less likely to be future oriented. The model also provides a potential explanation for the variability and fluctuation of symptoms seen in ADHD by making a distinction between sustained attention that is contingency-shaped and context dependent and that which is governed by executive functions that require self-control (Barkley, 1997b). The implication of behavioral disinhibition is that children with ADHD will be more likely than those without ADHD to behave in ways that elicit immediate reinforcement (whether the reinforcement is positive or negative). Children with ADHD are less able to “stop, look, listen” and have more difficulty “waiting” when compared with same-aged peers without ADHD (Schweitzer & Sulzer-Azaroff, 1995). Perseveration of ongoing responses and poor interference control also are components of behavioral disinhibition often seen in children with ADHD. Perseveration of ongoing responses means that the child with ADHD is less able to interrupt an ongoing response or response pattern to “stop and think,” resulting in behavior that is less flexible and less likely to change as the context of the situation changes (Barkley, 1997b). Poor interference control results in the child with ADHD being more subject to distraction from both external or environmental factors, as well as internal factors such as task irrelevant thoughts.
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Figure 2. Revised diagram of the hybrid model of executive functions shows the numerous cognitive deficits predicted to be associated with deficits in behavioral inhibition in ADHD. [From Barkley (1997b). Copyright 1997 by The Guilford Press. Reprinted by permission.]
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Poor working memory resulting from behavioral disinhibition means that the child with ADHD has limited insight, is less likely to learn from the behavior of others, and is less oriented to time (Barkley, 1997b). Much to the irritation of those around them, children with ADHD are less likely to use the nonverbal cues of others to guide their own behavior. They are more likely to get in trouble for the same behavior over and over, because they simply fail to recall that they got in trouble before. It is not that they do not know appropriate behavior, they just tend to act before they think. Poor working memory also affects the sense of time in children with ADHD (Barkley, 1997b). Often poor forethought and poor planning are evident as these children wait until a deadline approaches before beginning a project. Children with ADHD are often renowned for being late or not showing up for classes or appointments. Situations that require a waiting period, taking turns, or delayed responding are frustrating for the child with ADHD because they appear to perceive time as moving more slowly than those without ADHD (Barkley, Koplowitz, Anderson, & McMurray, 1997; Sonuga-Barke, Williams, Hall, & Saxton, 1996). Diminished sense of time also affects the performance of social skills (sharing, taking turns, etiquette) as well as other adaptive behaviors such as health consciousness and concerns for safety. Again, the tendency to act without thinking puts the child with ADHD at risk for physical injury and poor health. The hybrid model predicts that children with ADHD are delayed in the internalization of speech (Barkley, 1997b). They continue to exhibit audible self-directed speech when compared with their peers without ADHD. Delayed internalization of speech also affects rule-governed behavior. Children with ADHD are less likely to follow the rules of others and are less likely to generate their own rules, resulting in behavior that appears thoughtless, unintentional, and impulsive. Immature self-regulation of affect, motivation, and arousal results as a consequence of behavioral disinhibition (Barkley, 1997b). Poor emotional self-control results in the child with ADHD expressing emotions in a way that appears extreme, self-serving, or even rude. Lack of insight prevents the child with ADHD from considering other people’s feelings apart from his or her own. Children with ADHD also are less able to motivate themselves to persist in goal-directed activities that require delayed gratification. Self-motivation is more difficult as the delay in gratification becomes longer (Sonuga-Barke, Taylor, Sembi, & Smith, 1992). Impaired reconstitution results in behavior that is less complex and flexible (Barkley, 1997b). The hybrid model predicts that children with ADHD are less able to analyze and synthesize previously acquired behavioral sequences for responding to novel situations. Consequently, children
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with ADHD take longer to assimilate complex behavioral sequences that would allow them to exhibit appropriate behavior. They frequently have trouble learning from their own mistakes, much less the mistakes of others. The final prediction of the hybrid model is that behavioral disinhibition gives rise to secondary deficits in the executive functions and results in reduced motor control, fluency, and syntax (Barkley, 1997b). Basically, this prediction indicates that the child with ADHD will exhibit more task irrelevant activity than normal. Motor activity is more subject to the external environment and is less goal-directed. This prediction helps to explain the high activity levels described by parents and teachers of children with ADHD. FUTURE IMPLICATIONS Although previous research provides validation for many of the predictions made by the model, other predictions remain untested (Barkley, 1997b; Oosterlaan, Logan, & Sergeant, 1998). For instance, no one has fully tested the prediction that impairment of behavioral inhibition leads to a secondary impairment in working memory and, more specifically, the sense of time. The sense of time that working memory promotes affects adaptive functioning across a variety of settings on a daily basis. Children are expected to function adequately on time-bound tasks and exhibit goal-directed behavior by a certain age. The predictions of the hybrid model provide a useful explanation for the difficulties that children with ADHD experience if they have an impaired sense of time. That knowledge would be clinically useful for the myriad of disciplines responsible for developing interventions and support programs for children with ADHD. Health-promoting behavior, which often requires selfcontrol, is contingent on the development of a sense of time. If the predictions in this model are supported, interventions that help to develop the sense of time and foster a child’s ability to “stop, look, and listen” could improve health maintenance and decrease health–risk behavior in the ADHD population. REFERENCES Aman, M. G. (1984). Hyperactivity: Nature of the syndrome and its natural history. Journal of Autism and Developmental Disorders, 14(1), 39–56. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. Barkley, R. A. (1976). Predicting the response of hyperkinetic children to stimulant drugs: A review. Journal of Abnormal Child Psychology, 4(4), 327–348. Barkley, R. (1981). Hyperactive children: A handbook for diagnosis and treatment. New York: Guilford Press.
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Barkley, R. (1997a). Behavioral inhibition, sustained attention, and executive functions: Constructing a unifying theory of ADHD. Psychological Bulletin, 121(1), 65–94. Barkley, R. A. (1997b). ADHD and the nature of self-control. New York: Guilford Press. Barkley, R. A. (1998a, November 6). Attention-deficit hyperactivity disorder (Internet). Scientific American. Barkley, R. A. (1998b). Attention-deficit hyperactivity disorder: A handbook for diagnosis and treatment (2nd ed.). New York: Guilford Press. Barkley, R. A., Fischer, M., Edelbrock, C. S., & Smallish, L. (1990). The adolescent outcome of hyperactive children diagnosed by research criteria: An 8-year prospective follow-up study. Journal of the American Academy of Child and Adolescent Psychiatry, 29(4), 546–557. Barkley, R. A., Koplowitz, S., Anderson, T., & McMurray, M. B. (1997). Sense of time in children with ADHD: Effects of duration, distraction, and stimulant medication. Journal of the International Neuropsychological Society, 3, 359–369. Becker, R. D. (1974). Minimal cerebral (brain) dysfunction—clinical fact or neurological fiction? The syndrome critically re-examined in the light of some hard neurological evidence. The Israel Annals of Psychiatry and Related Disciplines, 12(2), 87–106. Biederman, J., Faraone, S. V., Mick, E., Spencer, T., Wilens, T., Kiely, K., Guite, J., Ablon, J., & Reed, E. W., R. (1995). High risk for attention deficit hyperactivity disorder among children of parents with childhood onset of the disorder: A pilot study. American Journal of Psychiatry, 152, 4312–4435. Block, G. H. (1977). Hyperactivity: A cultural perspective. Journal of Learning Disabilities, 10, 236–240. Bradley, C. (1937). The behavior of children receiving benzedrine. American Journal of Psychiatry, 94, 577–585. Bronowski, J. (1977). Human and animal languages. In A sense of the future (pp. 104– 131). Cambridge, MA: MIT Press. Douglas, V. I. (1972). Stop, look, and listen: The problem of sustained attention and impulse control in hyperactive and normal children. Canadian Journal of Behavioural Science, 4, 259–282. Fuster, J. M. (1997). The prefrontal cortex: Anatomy, physiology, and neuropsychology of the frontal lobe. Philadelphia: Lippincott-Raven. Gittelman, R., Mannuzza, S., Shenker, R., & Bonagura, N. (1985). Hyperactive boys almost grown up. Archives of General Psychiatry, 42, 937–947. Goldman, L. S., Genel, M., Bezman, R. J., & Slanetz, P. J. (1998). Diagnosis and treatment of attention-deficit/hyperactivity disorder in children and adolescents. Journal of the American Medical Association, 279(14), 1100–1107. Goldman-Rakic, P. S. (1995). Architecture of the prefrontal cortex and the central executive. In J. Grafman, K. J. Holyoak, & F. Boller (Eds.), Annals of the New York Academy of Sciences: Structure and functions of the human prefrontal cortex, 769, 71–83. Goodyear, P., & Hynd, G. (1992). Attention deficit disorder with (ADD/H) and without (ADD/WO) hyperactivity: Behavioral and neuropsychological differentiation. Journal of Clinical Child Psychology, 21, 273–304. Hassler, F. (1992). The hyperkinetic child: A historical review. Acta Paedopsychiatrics, 55, 147–149.
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Jaksa, P. (1998). Fact sheet on attention deficit-hyperactivity disorder (ADHD/ADD), [Internet: www.add.org/content/abc/factsheet.htm] (11-04-1998). Kahn, E., & Cohen, L. H. (1934). Organic driveness: A brain-stem syndrome and an experience. New England Journal of Medicine, 210(14), 748–756. Levin, P. M. (1938). Restlessness in children. Archives of Neurology and Psychiatry, 39, 764–770. Mariani, M. A., & Barkley, R. (1997). Neuropsychological and academic functioning in preschool boys with attention deficit hyperactivity disorder. Developmental Neuropsychology, 13(1), 111–129. McCarthy, G., Puce, A., Constable, R. T., Krystal, J. H., Gore, J. C., & Goldman-Rakic, P. (1996). Activation of human prefrontal cortex during spatial and nonspatial working memory tasks measured by functional MRI. Cerebral Cortex, 6, 600–611. Oosterlaan, J., Logan, G. D., & Sergeant, J. A. (1998). Response inhibition in AD/HD, CD, comorbid AD/HD+CD, Anxious, and Control Children: A meta-analysis of studies with the stop task. Journal of Child Psychology and Psychiatry, 39(3), 411–425. Pennington, B. F., Groisser, D., & Welsh, M. C. (1993). Contrasting cognitive deficits in attention deficit hyperactivity disorder versus reading disability. Developmental Psychology, 29(3), 511–523. Quay, H. C. (1987). The behavioral reward and inhibition systems in childhood behavior disorder. In L. M. Bloomingdale (Ed.), Attention deficit disorder: III. New research in treatment, psycho-pharmacology, and attention (pp. 176–186). New York: Pergamon Press. Rutter, M. (1977). Brain damage syndromes in childhood: Concepts and findings. Journal of Child Psychology and Psychiatry, 18, 1–21. Satterfield, J., Hoppe, C. M., & Schell, A. M. (1982). A prospective study of delinquency in 110 adolescent boys with attention deficit disorder and 88 normal adolescent boys. American Journal of Psychiatry, 139(6), 795–798. Schrag, P., & Divoky, D. (1975). The myth of the hyperactive child. New York: Pantheon Books. Schweitzer, J. B., & Sulzer-Azaroff, B. (1995). Self-control in boys with attention deficit hyperactivity disorder: Effects of added stimulation and time. Journal of Child Psychology and Psychiatry, 36(4), 671–686. Smith, E. E., Jonides, J., & Koeppe, R. A. (1996). Dissociating verbal and spatial working memory using PET. Cerebral Cortex, 11, 11–20. Solomons, G. (1965). The hyperactive child. Journal of Iowa Medical Society, 55, 464–469. Sonuga-Barke, E. J. S., Taylor, E., Sembi, S., & Smith, J. (1992). Hyperactivity and delay aversion: I. The effect of delay on choice. Journal of Child Psychology and Psychiatry, 33, 387–398. Sonuga-Barke, E. J. S., Williams, E., Hall, M., & Saxton, T. (1996). Hyperactivity and delay aversion III: The effect on cognitive style of imposing delay after errors. Journal of Child Psychology and Psychiatry, 37(2), 189–194. Stewart, M. A. (1970). Hyperactive children. Scientific American, 222, 94–98. Strecker, E., & Ebaugh, F. G. (1924). Neuropsychiatric sequelae of cerebral trauma in children. Archives of Neurology and Psychiatry, 12, 443–453. Weiss, G., Hechtman, L., & Perlman, T. (1978). Hyperactives as young adults: School, employer, and self-rating scales obtained during ten-year follow-up evaluation. American Journal of Orthopsychiatry, 48(3), 438–445.
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