Reprinted from Thomas Armstrong, “Attention Deficit Hyperactivity Disorder in Children: One Consequence of the Rise of Technologies and the Demise of Play,” in Sharna Olfman (ed.) All Work and No Play…How Educational Reforms Are Harming Our Preschoolers. Westport Ct.: Praeger, 2003, pp. 161-16.
Over the past thirty years, Attention Deficit Hyperactivity Disorder (ADHD) has emerged from the obscurity of cognitive psychology research laboratories to become the leading psychiatric disorder of childhood in the United States. A recent study conducted at the Mayo Clinic stated that as many as 7.4 to 16 percent of all children and adolescents suffer from this disorder (Barbaresi et a1., 2002). The American Psychiatric Association (1994) has established the following criteria for the ADHD diagnosis: The patient must exhibit behaviors related to inattention (e.g., “may fail to give close attention to details or may make careless mistakes in schoolwork or other tasks,” p. 78) or hyperactivity/impulsivity (e.g., “they fidget with objects, tap their hands and shake their feet excessively,” p. 79). In addition, symptoms must persist for at least six months, be maladaptive and inconsistent with developmental level, impair social or academic functioning, be present in the child before the age of seven, and have influenced behavior in two or more settings (e.g., school and home).
There is wide consensus among scientists, physicians, psychologists and educators that ADHD is a genetically influenced, neurologically based psychiatric disorder. Specific genes are believed to give rise to dysfunction in the frontal lobes of the cerebral cortex and their connections to subcortical structures in the limbic system and the cerebellum. The medical literature also earmarks disrupted dopaminergic pathways in the etiology of ADHD (Barkley, 1990,2002; Giedd et a1., 1994; LaHoste et a1., 1996). Despite the widely held belief that ADHD is a medical disorder, there are compelling reasons to question this assumption (see, for example, McGuinness, 1989; Reid, Maag, & Vasa, 1993; Armstrong, 1997, 1999; Nyland, 2002). First, there is not a single diagnostic test currently available that can definitively establish the presence of ADHD as a neurological disorder. As New York psychiatrist Esther Wender (2002, p. 210) states in her editorial on the Mayo Clinic study: “[ADHD] is identified by a cluster of typical behaviors and has no definitive biological marker. And because the condition cannot be objectively defined, the decision to treat will also be based on diagnostic uncertainties. The published diagnostic criteria lend an aura of objectivity to the diagnosis, but the application of these criteria is based on subjective judgments regarding the accuracy of information given by parents and teachers.”
Second, many of the studies that have sought to establish a neurological basis for ADHD have used brain-scan technologies that are still in their infancy, such as Positron Emission Tomography (PET) and Functional Magnetic Resonance Imaging (MRI). Studies of childhood mental disorders that utilize these technologies are frequently riddled with methodological difficulties, such as relatively small subject populations, heterogeneous samples, and problems in measuring the neurological correlates of complex behaviors under highly controlled and artificial laboratory conditions. These factors should temper our ready acceptance of these results (Hendren, DeBacker, & Pandin, 2000).
Third, when brain-imaging results reveal differences in a child’s brain functioning or structure, it is typically assumed that these differences are innate and immutable, rather than a response to environmental conditions. Brain-scan images are routinely interpreted as if they were neurological fingerprints: indelible and intractable. However, research on other psychiatric conditions such as Obsessive Compulsive Disorder (OCD) has demonstrated that psychotherapeutic interventions can significantly alter brain scan patterns (Schwartz, Stoessel, Baxter, Martin, & Phelps, 1996). Furthermore, there is compelling evidence that environmental factors such as stress and trauma may trigger neurochemical events in the brain that impair frontal lobe structure and functioning in children (Perry & Pollard, 1998; Arnsten, 1999). These findings suggest that nature and nurture work together in an intricate way to produce behaviors such as those seen in ADHD. Therefore, we must question whether ADHD is “in” the child as a fixed neurological disorder, or whether instead, ADHD symptoms reflect dysfunctional relationships between the child and the environment. There are, in fact, a number of studies, discussed below, that support this premise.
Research studies have demonstrated that children’s ADHD symptoms decrease under a variety of environmental conditions, including when they are engaged in one-on-one learning experiences, when they’re being paid to do tasks, when they have access to novel or highly stimulating activities, when they’re in control of the pace of learning experiences, and when they’re interacting with male authority figures (Barkley, 1990; McGuinness, 1985; Zentall, 1980; Sykes, Douglas, & Morgenstern, 1973; Sleator & Ullman, 1981). From this we can infer that symptoms of ADHD in children might increase when the opposite environmental conditions pertain, such as when they’re performing in boring or low-stimulation environments, when they’re not receiving a meaningful reward for their efforts, and when they’re powerless to control the pace of learning tasks. Indeed, if these conditions are present in a child’s home environment from birth, it is reasonable to suspect that they could lay the groundwork for the disorder itself.
In a survey of ADHD-diagnosed and “normal” children aged six to seventeen, the odds of a child being diagnosed with ADHD increased in proportion to the extent that they came from a family characterized by adversity, including severe marital discord, low social class, large family size, paternal criminality, maternal mental disorder, and foster care placement (Biederman et al., 1995). Other studies have demonstrated that the quality of caregiving in early childhood predicts distractibility (a key symptom of ADHD) better than early biological markers or temperament, and that a strong overlap exists between symptoms of ADHD and Post-Traumatic Stress Disorder (PTSD) in children, suggesting that early sexual, physical, and/ or emotional abuse may play an important role in the origin of ADHD symptoms for some children (Carlson, Jacobvitz, & Sroufe, 1995; Weinstein, Staffelbach, & Biaggio, 2000).
If we expand our exploration of the role of the environment in creating ADHD symptoms to include broader sociocultural factors, we might consider the possibility that the disorder of ADHD is itself a cultural phenomenon that has been socially constructed as a “neurological disorder.” There is compelling historical precedence for this type of construction. In the 1850s, for example, a Louisiana physician named Samuel A. Cartwright (1851) contributed a paper to the New Orleans Medical and Surgical Journal, in which he stated that he had discovered a new medical disorder that he named “drapetomania” (an obsession with fleeing). Dr. Cartwright believed that this” disorder” afflicted large numbers of runaway slaves, and that with proper identification and treatment, they could learn to live productive and successful lives back on the plantation (Cartwright, 1851). More recently (1973), the American Psychiatric Association (which played a leading role in defining and legitimizing the diagnosis of ADHD) rescinded its diagnosis of “homosexuality” as a pathological condition. Clearly, there is ample precedent for the influence of sociocultural context upon the thinking and discourse of mental health professionals in this country. As social values and norms change over time, so do the classifications of deviance. It has even been suggested, by the former president of the American Psychological Association, Nicholas Hobbs (1975), that society defines itself in part by the categories of deviance it assigns to its members, especially to its children.
In this spirit, a number of educators and mental health professionals have expressed concern that the diagnosis of ADHD in children is an attempt to medicalize behaviors that should more properly be seen as natural responses to the broader social and cultural environment. Thirty years ago, during the social upheavals of the 1960s and early 1970s, Harvard professor Lester Grinspoon observed that: “Children growing up in the past decade have seen claims to authority and existing institutions questioned as an everyday occurrence. . . Teachers no longer have the unquestioned authority they once had in the classroom. . . . The child, on the other side, is no longer so intimidated by whatever authority the teacher has.. . . Hyperkinesis [a term used to describe ADHD symptoms in the 1960s and 1970s], whatever organic condition it may legitimately refer to, has become a convenient label with which to dismiss this phenomenon as a physical’ disease’ rather than treating it as the social problem it is. (Grinspoon & Singer, 1973, pp. 546-547)
Since that time, the United States has seen even greater changes in its social makeup and values, with family upheaval on the rise, and individual time spent by working parents directly engaged with their children decreasing. One study suggested that fathers spend an average of only five minutes per day interacting with their adolescent children (Csikszentmihalyi, 2000). Additionally, children in contemporary society are subject to multiple stressors, including a faster pace of life, an increasingly regimented school system, neighborhood violence, and terrorist threats. As Antoinette Saunders and Bonnie Remsberg (1986, p. 25) point out in their book, The Stress-Proof Child: “Our children experience the stress of illness, divorce, financial problems, living with single parents, sex, drugs, sensory bombardment, violence, the threat of nuclear war-a long, long list. The effect can be overwhelming.” Since symptoms of stress include restlessness, difficulty concentrating, and irritable behavior-in other words, the same behaviors characteristic of ADHD, it seems reasonable to suspect that a link may exist between these larger social forces and the increase in the number of children identified as ADHD over the past thirty years.
Among the many social trends in our culture that may contribute to the ADHD behaviors of hyperactivity, distractibility, and impulsivity in children, I would like to focus on two developments in particular: the rise of technologies and the demise of play. These two events should be looked at in relation to each other, for as children spend more time watching television, playing video games, surfing on the Internet, manipulating toys run by computer chips, and engaging in other technologically based activities, there is less time available for them to engage in non-adult-supervised open-ended play situations such as pretense play (where children use their imaginations to make up and act out novel scenarios) and rough-and-tumble play (where children wrestle, fight, climb, run, build, and take part in other unstructured, whole-body activities). The link between the rise of technologies and the demise of play is well illustrated by University of Pennsylvania play expert Brian Sutton-Smith (in Hansen, 1998, p. 25), who writes: “American children’s freedom for freewheeling play once took place in rural fields and city streets, using equipment of their own making. Today, play is increasingly confined to back yards, basements, playrooms and bedrooms, and derives much of its content from video games, television dramas, and Saturday morning cartoons.”
The Crucial Role of Play for Healthy Brain Development. As noted earlier, ADHD is typically viewed by the scientific community as a neurological disorder resulting from dysfunction in the frontal lobes of the cerebral cortex and their connections to subcortical structures in the limbic system and the cerebellum (Barkley, 1990,2002; Giedd et al., 1994; LaHoste et aI., 1996). Thus, the executive functions of the frontal lobes are not able to properly regulate and inhibit the emotional and motor features of the limbic system and cerebellum. Put in the context of play, the limbic system enables the child’s spontaneity and vitality of physical and emotional expression and the cerebellum enables a wide range of motor experiences in play, whereas the frontal cortex serves to inhibit or redirect those impulsive and motoric energies along socially appropriate channels through planning, empathy, focused attention, language, and reflection.
At first it may seem that free play is most obviously limbic systemdriven, as children express their vitality and spontaneity in unpredictable and sometimes explosive ways. However, I was recently reminded of the role of inhibition, and the redirection of impulses in free play, after observing two primary-level boys engaged in a bit of rough-andtumble play in a museum. The two were alternately thrusting their hands at each other and feigning to strike in an attempt to “fake out” the other person. Clearly in this aggressive play activity, there was plenty of inhibition involving suppressing the motor impulse to strike when it was strategically and/or socially appropriate to do so. If you observe any group of children engaged in healthy play, you will notice this element of inhibition being worked out, as they seek to adjust their own roles, postures, language, and imaginations to those of the other children in their play group. The more impulsive aspects of playfulness, which are directed by the limbic system (and come out as manic and unsocialized “play” in many children labeled ADHD), seem to be modulated and “civilized” by the more socialized and languagedriven aspects of play that are directed by the frontal lobes.
There is evidence that the kinds of social adaptations and learning experiences that young children acquire through play actually modify brain structure and functioning by creating new synaptic connections in the neocortex (Diamond & Hopson, 1998). It has even been suggested by some researchers that the evolution of the frontal lobes in primates occurred in part as a result of the experience of play (Furlow, 2001). Neuroscientist Jaak Panksepp (1998, p. 96) writes: “Indeed, ‘youth’ may have evolved to give complex organisms time to play and thereby exercise the natural skills they will need as adults. We already know that as the frontal lobes mature, frequency of play goes down, and animals with damaged frontal lobes tend to be more playful. . . Might access to rough-and-tumble play promote frontal lobe maturation?” Panksepp suggests that “[t]he explosion of ADHD diagnoses may largely reflect the fact that more and more of our children no longer have adequate spaces and opportunities to express this natural biological need-to play with each other in vigorous rough-and-tumble ways, each and every day” (p. 91). If children don’t have the opportunity to work out the relationship between limbic system ex-plosiveness and frontal lobe appropriateness through normal play situations, this may indeed result in failure of the frontal lobes to fully mature, and set the neurological stage for the kinds of frontal lobelimbic system dysfunctions described in the ADHD literature.
A recent report issued by the National Association for Sport and Physical Recreation recommended that children engage in one to two hours of physical activity every day, yet increasingly schools are cutting back on physical education programs and recess periods in order to dedicate more time to academic achievement (often spent in front of a computer), and to make matters worse, research suggests that children are not making up the physical activity they are losing in school by increasing their physical activities after school (Dale, Corbin, & Dale, 2000). Providing opportunities for physical release may be of critical importance for children with ADHD symptoms. A recent study has demonstrated that children identified as ADHD show improvement after participating in play activities in natural settings, and that the “greener” a child’s play area (that is, the more it takes place outdoors), the less severe his or her attention-deficit symptoms (Taylor, Kuo, & Sullivan, 2001).
The Rise of Technologies. Two years ago, while traveling in Asia, I had a layover at the Tokyo Narita Airport. While wandering around, I noticed that there was a “Children’s Play Room” and went in to take a look. There were no play spaces, open spaces, gymnastic equipment, or other tools for pretense or rough-and-tumble play. The “play space” consisted solely of computer terminals. Every single child was sitting in front of an individual computer station utilizing a software program. (On a more recent trip, I noticed that a few Lego plastic building blocks had made their appearance in a back corner of the room.)
My visit to the “Children’s Play Room” in Tokyo stunned me, and led me to realize how much the meaning of children’s play has changed over the past several decades, from the kinds of open-ended active explorations described above, involving the broad use of imagination, physical expression, complex social interactions, and creative language, to “technological play,” which is generally passive (children sitting in front of computer terminals making only occasional small motor movements with their fingers on the keyboard or joystick), close-ended (the software program structures the flow of play, even when it is highly interactive), unimaginative (the software images are the products not of the children’s imagination but of Silicon Valley minds concerned with generating profit), and lacking in opportunities for language development and social interaction (children, even when playing together, do not face each other to relate, but rather are all turned toward the screen). There are virtually no opportunities in this kind of context for an active interplay between the child’s spontaneous vitality-controlled by the limbic system- and the inhibition and redirection of impulses through social interaction, language expression, and reflection- mediated by the developing frontal lobes. Thus, one can hypothesize that such an environment could create the very dysfunction between the limbic system and the frontal lobe system that is hypothesized to cause or exacerbate the symptoms that compose the ADHD diagnosis.
The popular children’s movie Monsters, Inc. illustrates how children have been influenced by our technologically sophisticated, violent media culture. Monsters, Inc. is a movie about a group of monsters that work for a utility company. The” affable” monsters make children scream by walking into their bedrooms at night, and then they bottle up the energy in the screams to use as an energy source in their subterranean monster world. A crisis erupts however, when it becomes apparent that children aren’t screaming as much as they did before, and as a result the monsters’ energy supply is becoming depleted. The problem is that “kids don’t scare so easily anymore.” As a result, the monsters need to up the ante by terrorizing the children even more than before (Mitchell, 2001).
The movie Monsters, Inc. highlights the fact that children are “harder to scare” in today’s violent media culture, and thus require even higher doses of fright, or at least higher levels of stimulation, to get their attention. In my opinion, the real monsters in children’s lives are the media advertisers and programmers who, over the past fifty years, have gradually perfected the art of grabbing people’s attention to sell products and services that “fuel” the entertainment machines of America. To witness the magnitude of this change, one has only to view a television program from the early 1950s-let’s say, The Honeymooners-and track the amount of time that the show stays fixed on a given scene with an unchanging camera view. In programs created a few decades ago, most of the camera shots stay fixed for several seconds on one scene. Contrast this with a current commercial or a program on MTV, and you will soon discover that contemporary scenes usually shift in increments of less than one second. In 1992, CBS News attempted a novel experiment in their political coverage of the presidential elections. They began using “30 second sound bites” in an attempt to provide greater “in-depth coverage” to the political candidates’ views. This experiment was stopped after a short while because it was concluded that the average adult viewer was unable to sustain his attention for that long a period of time, and the network went back to the standard seven-second sound bite (Berke, 1992).
One of the reasons for the change from stationary camera shots to rapidly shifting ones in television programs is a concomitant change in our “orienting response,” a mechanism first described by Russian physiologist Ivan Pavlov in 1927. The orienting response is our instinctive biological reaction to any sudden or novel stimulus, and includes dilation of the blood vessels to the brain and constriction of blood vessels to major muscle groups. Mental arousal becomes heightened (alpha waves in the brain are blocked for a few seconds) and visual and auditory perceptions are sharpened. The orienting response evolved to help protect Homo sapiens from sudden environmental changes, such as the threat of nearby predators. Television advertisers have discovered this powerful biological response and are using it to sell products. By using loud noises, sudden camera shifts, violent content, and other novel stimuli, they are manipulating these evolutionary structures in the service of non-life-threatening stimuli, for example, programming and commercials (Reeves & Thorson, 1986).
However, like the story of “The Boy Who Cried Wolf,” we eventually habituate to these attention-grabbing ploys as we learn that there is no real threat present. Viewers become “harder to scare,” or at least harder to bring back to the screen. This necessitates even more novel stimuli, sudden shifts, explosions, and the like, to grab the attention of the viewer back again by activating their orienting response. Over a period of years, then, this process has gradually created faster, sharper, louder, and more violent stimuli in television, movies, and video games. And among consumers of media, it has behaviorally modified the orienting response so that much higher levels of stimulation are required to obtain the same biological effects that the 1950s sitcom I Love Lucy or the 1960s video game Pong used to produce. (It is interesting to note that the first movies of trains traveling toward the viewer in the early twentieth century sent audiences screaming out of the theaters.)
Thus, the rise of technologies and the needs of the market economy have apparently created a “short-attention-span” culture. A study conducted in the 1980s tracked the changes that occurred in a mountain community in Canada after it acquired access to television for the first time. Over a period of two years, the adults and children in that community became less able to persevere at tasks, less able to engage in creative problem solving, and less tolerant of unstructured time (Williams, 1986). It should hardly be surprising that today’s media-fed children, growing up on MTV, video games, the Internet, and violent television, should have also developed short attention spans. Thirty-five years ago, Marshall McLuhan described the first wave of this trend when he spoke of a generation of kids whose worldview was no longer based on plodding, one-step-at-a-time thinking, but rather on instantaneous flashes of immediate sensory data (McLuhan & Fiore, 1967). Around the same time, media expert Tony Schwartz wrote: “Today’s child is a scanner, his experience with electronic media has taught him to scan life the way his eye scans a television set or his ears scan auditory signals from a radio or stereo speaker” (1973, pp. 110-111). It may be no coincidence that Attention Deficit Hyperactivity Disorder was formulated as a disability category in the early 1970s, at the same time that McLuhan and Schwartz were making these observations.
The medical literature has targeted disrupted dopaminergic pathways as a key element in the etiology of ADHD. Dopamine plays a central role in the modulation of stimulus seeking or reward seeking. When dopamine transmission is interfered with, an individual can develop an insatiability for rewards, or a need for higher stimulation levels than normal. This, in fact, is what many researchers have typically seen in children identified as ADHD: they require higher levels of stimulation than the average person. Ritalin and other shortacting stimulants help to provide this missing stimulation in chemical form. Some researchers have found that nondrug forms of stimulation-such as music, color, and lights-also help to provide an optimal level of stimulation for these understimulated children and thereby calm them down (Zentall, 1975, 1993; Zentall & Zentall, 1983; Zentall, Hall, & Lee, 1998). These findings must be reexamined in light of the heightened media-fed orienting response described above, because it may be that the rising crescendo of media stimulation in children creates, or at the very least contributes, to the need for higher levels of stimulation at the dopaminergic level in children diagnosed as ADHD. Indeed, well over a thousand studies have demonstrated that exposure to violent programming among children and adolescents creates violent behavior (Johnson, 2002; Sappenfield, 2002). In addition, other physiological responses to high-stimulation television and video-game experiences have been documented in the literature, including “TV-induced fright,” “video-game epilepsy,” and the possibility of television addiction on a par with substance abuse (Fylan, Harding, & Webb, 1999; Valkenburg, Cantor, & Peters, 2000; Kubey & Csikszentmihalyi, 2002).
In light of the above research on the impact of the demise of play and the rise of screen technologies on children’s lives, we are compelled to ask what the consequences of these sociacultural developments could be for a child in today’s world. What is likely to happen when a child is deprived of natural play experiences that facilitate the harmonious coordination of the limbic system and the frontal lobes of the brain, and instead is immobilized in front of a video game, computer, or television screen and exposed to violent or other highstimulus material that activates his innate orienting response with no opportunity to respond motorically or emotionally to these stimuli except through a few twitches of a joystick, a keyboard, or a channel changer? It is hardly surprising that children might respond to the absence of a vital developmental force (play) and relentless exposure to devitalizing technological “mechanism manipulation” (TV, video games, computers) by becoming inattentive, hyperactive, and impulsive. Indeed, it is perhaps a very natural result of these very unnatural cultural developments.
Unfortunately, the ADHD community of researchers are for the most part ill-disposed toward investigating sociocultural influences on symptoms, and remain confident in the belief that ADHD is a culture-free neurological disorder of genetic origin. A recent consensus statement on ADHD signed by seventy-four international scientists working in the ADHD field assails those who suggest that “behavior problems associated with ADHD are merely the result of [among other things] excessive viewing of TV or playing of video games.” It concludes: “To publish stories that ADHD is. . . merely a conflict between today’s Huckleberry Finns and their caregivers is tantamount to declaring the earth flat, the laws of gravity debatable, and the periodic table in chemistry a fraud” (Barkley, 2002, p. 90). It remains to be seen whether thoughtful people will accept this highly positivist view of children and behavior, or will instead consider the possibility that historical events and cultural trends may also have powerful effects upon the brains and behaviors of our children.
American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author.
Armstrong, T. (1997). The myth of the A.D.D. child: 50 ways to improve your child’s behavior span without drugs and attention, labels, or coercion. New York: Plume.
Annstrong, T. (1999). ADD/ADHD alternatives in the classroom. Alexandria, VA: Association of Supervision and Curriculum Development.
Arnsten, A.F.T. (1999). Development of the cerebral cortex: XIV. Stress impairs prefrontal cortical function. Journal of the American Academy of Child & Adolescent Psychiatry, 38, 220-222.
Barbaresi, W, et al. (2002, March). How common is Attention-Deficit-Hyperactivity Disorder? Archives of Pediatric and Adolescent Medicine, 156,217-224.
Barkley, RA. (1990). Attention Deficit Hyperactivity Disorder: A handbook for diagnosis and treatment. New York: Guilford Press.
Barkley, RA. (2002, June). International consensus statement on ADHD.Clinical Child and Family Psychology Review, 5(2), 89-111.
Berke, RL. (1992, July 11). Sound Bites Grow at CBS, Then Vanish. New York Times, p. L7.
Biederman, J., Milberger,S., Faranoe, S.V., Kiely, K., Guite, J., & Mick, J., et al. (1995, March). Family-environment risk factors for Attention-Deficit Hyperactivity Disorder. Archives of General Psychiatry, 52, 464-469.
Carlson, E.A., Jacobvitz, D., & Sroufe, L.A. (1995, February). A developmental investigation of inattentiveness and hyperactivity. Child Development, 66(1),37-54.
Cartwright, S.A. (1851, May). Report on the diseases and physical peculiarities of the Negro race. The New Orleans Medical and Surgical Journal, 7, 691-716.
Csikszentmihalyi, M. (2000, April 19). Education for the 21st century. Education Week, 46.
Dale, D., Corbin, C.B., Dale, K.S. (2000, September). Restricting opportunities to be active during school time: Do children compensate by increasing physical activity levels after school? Research Quarterly for Exercise and Sport, 71, 240.
Diamond, M., & Hopson, J. (1998). Magic trees of the mind: How to nurture your child’s intelligence, creativity, and healthy emotions from birth through adolescence. New York: Dutton.
Furlow, B. (2001, June 9). Kids need the playground just as much as the classroom: Having fun builds bigger, better brains. New Scientist.
Fylan, F., Harding, G.E, & Webb, RM. (1999). Mechanisms of video-game epilepsy. Epilepsia, 40, 28-30.
Giedd, J.N., Castellanos, EX., Casey, B.J., Kozuch, B.A., King, A.c., & Hamburger, S.D., et al. (1994, May). Quantitative morphology of the corpus callosum in Attention Deficit Hyperactivity Disorder. American Journal of Psychiatry, 151, 665-668.
Grinspoon L., & Singer, S.B. (1973, November). Amphetamines in the treat ment of hyperkinetic children. Harvard Educational Review, 43, 546-547.
Hansen, L.A. (1998, March/April) Where we play and who we are. Illinois Parks and Recreation, 29(2), 22-25.
Hendren, RL., DeBacker, I., & Pandin, G.J. (2000, July). Review of neuroimaging studies of child and adolescent psychiatric disorders from the past 10 years. Journal of the American Academy of Child & Adolescent Psychiatry, 39, 815-828.
Hobbs, N. (1975). The futures of children. San Francisco, CA: Jossey-Bass.
Johnson. J.G., et al. (2002). Television viewing and aggressive behavior during adolescence and adulthood. Science, 295, 2468-2471.
Kubey, R, & Csikszentmihalyi, M. (2002, February). Television addiction is no mere metaphor. Scientific American, 286(2), 64-80.
LaHoste, G.J., Swanson, J.M., Wigal, S.B., Glabe, Wigal T., & King, N., et al. (1996). Dopamine D4 receptor gene polymorphism is associated with Attention Deficit Hyperactivity Disorder. Molecular Psychiatry, 1, 121-124.
McGuinness, D. (1985). When children don’t learn. New York: Basic Books. McGuinness, D. (1989). Attention Deficit Disorder: The emperor’s clothes, animal “pharm” and other fiction. In S. Fisher & RE Greenberg (eds.), The limits of biological treatment for psychological distress (pp. 151-183). Hillsdale, NJ: Lawrence Erlbaum.
McLuhan, M., & Fiore, Q. (1967). The medium is the message. New York: Bantam.
Mitchell, E. (2001, November 2). Monsters of childhood with feelings and agendas. New York Times.
Nyland, D. (2002). Treating Huckleberry Finn: A new narrative approach to working with kids diagnosed ADD/ADHD. New York: Jossey-Bass.
Panksepp, J. (1998). Attention Deficit Hyperactivity Disorders, psychostimulants, and intolerance of childhood playfulness: A tragedy in the making? Current Directions in Psychological Science, 7,91-98.
Perry, B.D., & Pollard, R (1998). Homeostasis, stress, and adaptation: A neurodevelopmental view of childhood trauma. Child and Adolescent Psychiatric Clinics of North America, 7, 33-51.
Reeves, B., & Thorson, E. (1986). Watching television: Experiments on the viewing process. Communication Research, 13,343-361.
Reid, R, Maag, J.w., & Vasa, S.P. (1993). Attention Deficit Hyperactivity Disorder as a disability category: A critique. Exceptional Children, 60, 198-214.
Sappenfield, M. (2002, March 29). Mounting evidence links TV viewing to violence. Christian Science Monitor.
Saunders, A., & Remsberg, B. (1986). The stress-proof child. New York: Signet.
Schwartz, J.M., Stoessel, EW., Baxter, L.R, Jr., Martin, K.N., & Phelps, M.E.. (1996, February). Systematic changes in cerebral glucose metabolic rate after successful behavior modification treatment of obsessive compulsive disorder. Archives of General Psychiatry, 53, 109-113.
Schwartz, T. (1973). The responsive chord. Garden City, NY: Doubleday.
Sleator, E.K., & Ullman, R.L. (1981, January). Can the physician diagnose hyperactivity in the office? Pediatrics, 67, 13-17.
Sykes, D.H., Douglas, V.I., & Morgenstern, G. (1973). Sustained attention in hyperactive children. Journal of Child Psychology & Psychiatry & Allied Disciplines, 14,213-220.
Taylor, AE, Kuo, EE., & Sullivan, W.E. (2001, January). Coping with ADD: The surprising connection to green play settings. Environment and Behavior 33(1),54-77.
Valkenburg, P.M., Cantor, J., & Peters, AL. (2000, February). Fright reactions to television: A child survey. Communication Research, 27(1), 82-97.
Weinstein, D., Staffelbach, D., & Biaggio, M. (2000, April). Attention-Deficit Hyperactivity Disorder and Post-Traumatic Stress Disorder: Differential diagnosis in childhood sexual abuse. Clinical Psychology Review, 20, 359-378.
Wender, E.H. (2002, March). Editorial: Attention-Deficit/Hyperactivity Disorder: Is it common? Is it overtreated? Archives of Pediatric and Adolescent Medicine, 156, 209-210.
Williams, T. MacBeth. (1986). The impact of television: A natural experiment in three communities. Orlando, FL: Academic Press.
Zentall, S. (1975). Optimal stimulation as a theoretical basis for hyperactivity. American Journal of Orthopsychiatry, 45, 549-563.
Zentall, S. (1980). Behavioral comparisons of hyperactive and normally active children in natural settings. Journal of Abnormal Child Psychology, 8, 93-109.
Zentall, 5.5. (1993). Research on the educational implications of Attention Deficit Hyperactivity Disorder. Exceptional Children, 60, 143-153.
Zentall, 5.5., Hall, AH., & Lee, D.L. (1998). Attentional focus of students with hyperactivity during a word-search task. Journal of Abnormal Child Psychology, 26, 335-343.
Zentall, 5., & Zentall, T.R. (1983). Optimal stimulation: A model of disordered activity and performance in normal and deviant children. Psychological Bulletin, 94, 446-471.
For more information, see Thomas Armstrong, The Myth of the ADHD Child: 101 Ways to Improve Your Child’s Behavior and Attention Span Without Drugs, Labels, or Coercion (Tarcher/Perigee).
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