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by Thomas Armstrong
Table of Contents
Over the past 20 years, a new way of thinking about children with attention and behavior problems has gained widespread acceptance from all quarters of society. I am speaking of attention-deficit disorder (ADD) or attention-deficit-hyperactivity disorder (ADHD). Sparked by recent best sellers (Hallowell & Ratey, 1994a, 1994b) and coverage by the popular press (Glusker, 1997; Hales & Hales, 1996; Machan, 1996; Wallis, 1994), ADD/ADHD has become a household term for millions of Americans. Numerous popular guides for parents and teachers have appeared explaining what ADD/ADHD is, what causes it, and how it can be diagnosed and treated (e.g., Barkley, 1995; Cohen, M. W., 1997; Green & Chee, 1998). Researchers have published thousands of scientific papers in the past 20 years on a wide range of issues related to ADD/ADHD (Resnick & McEvoy, 1994). The disorder has received the support of mainstream psychiatry (American Psychiatric Association, 1994) and general medicine (Goldman, Genel, Bezman, & Slanetz, 1998), the stamp of governmental approval (Viadero, 1991), and widespread acceptance in U.S. schools (Smallwood, 1997).
What is ADD/ADHD? Or, more properly, What is the structure of the ADD/ADHD paradigm or world view? Although ADD/ADHD proponents may disagree on certain matters connected with the paradigm, such as whether ADD/ADHD is overdiagnosed (e.g., Ingersoll, 1995; Gordon, 1995), many professionals, parents, and other proponents of ADD/ADHD seem to have arrived at a consensus concerning the existence of a discrete disorder (or disorders). This consensus includes several basic assumptions:
In this chapter, I consider each of these assumptions and describe specific anomalies in them which, when taken as a whole, tend to call into question the essential credibility of the ADD/ADHD paradigm.
This tenet seems to be the foundation of the ADD/ADHD paradigm. To believe that ADD/ADHD is a biological disorder gives ADD/ADHD the stamp of approval of modern medicine, thus seeming to place it in a position unassailable by claims from fields with less cultural prestige, such as sociology, psychology, or education.
I'd like to focus on three major avenues of inquiry into the neurobiological basis for ADD/ADHD: positron emission tomography (PET) studies of cerebral glucose metabolism, magnetic resonance imaging (MRI) studies of structural differences between the so-called “ADHD brain” and the “normal” brain, and genetic studies.
The single event in the history of the ADD/ADHD paradigm that garnered the greatest attention pointing to ADD/ADHD as a medical disorder was perhaps the 1990 PET scan study by A. J. Zametkin and his colleagues at the National Institute of Mental Health (NIMH) in Bethesda, Maryland (Zametkin et al., 1990). In this study, researchers injected groups of adults identified as “hyperactive” and “normal” with radioactive glucose. Researchers then tracked this substance in the brain through positron emission tomography (PET) while the subjects engaged in a simple auditory-attention task. Results indicated that the “hyperactive” group had significantly less metabolism in areas of the prefrontal lobes of the brain that were important in the control of attention and motor activity. The study received significant attention in the media as “proof” that ADD/ADHD is a medical disorder (e.g., Elmer-DeWitt, 1990; Kolata, 1990; Squires, 1990).
When Zametkin and his colleagues (1993) attempted to replicate this study with adolescents three years later, however, they failed to find any significant global differences between “hyperactive” and “normal” groups. Similarly, attempts to find differences in brain metabolism of “hyperactive” girls also yielded no significant differences (Ernst et al., 1994). As Rapoport (1995) points out, “[because] PET scans can be cumbersome and difficult to do correctly ... it's been very hard to replicate findings.”
Even if researchers were to find significant differences between the cerebral glucose metabolic rate as measured in the PET scans of so-called “normal” and “ADHD” brains, one cannot be certain that these differences result from inherent neurological problems in the ADHD groups. Recent research suggests that the environment can have a big effect on brain metabolism. Jeffrey M. Schwartz and his colleagues at UCLA School of Medicine have been able to demonstrate systematic changes in cerebral glucose metabolic rates after successful behavior modification treatment of individuals described as having obsessive-compulsive disorder (Schwartz, Stoeseel, Baxter, Martin, & Phelps, 1996). If the environment can create positive changes in cerebral glucose metabolic rates, it may also be able to create negative changes.
As the next chapter shows, factors like stress, family discord, and cultural pressures may have a large role to play in the incidence of the kinds of behavior associated with ADD/ADHD among some people. Environmental factors may well interact with brain chemistry to create what looks like an “abnormal brain” but may be instead an intact brain responding to an “abnormal environment.”
The use of MRI technology has allowed researchers to look at structural features in the brains of people with so-called ADD/ADHD and those of “normals.” Using MRI technology, J. N. Giedd and his colleagues at NIMH compared sections of the midsagittal cross-sectional area of the corpus callosum (a collection of nerve fibers that connect right and left hemispheres) in 18 boys labeled ADHD with 18 matched “normal” boys (Giedd et al., 1994). They found that in the group identified as “ADHD,” the rostrum and rostral body regions of the corpus callosum were smaller at the 0.05 level of significance.
This study, and others like it, are used as indicators that people labeled ADHD have abnormal brains. Yet the study itself stated “no gross abnormalities were found in any subject” from the MRI measurements (Giedd et al., 1994, p. 666). Moreover, the study found no correlations between brain differences and measures of attention in the people identified as “attention deficit disordered.” The differences found in the “ADHD” group were subtle differences in only two of the seven regions measured—regions that relate to premotor functioning. Most important, even if these neuroanatomical differences do in fact exist (e.g., if future studies are able to replicate these findings) they could well represent just that—differences—and not necessarily disorders.
We should avoid pathologizing people so quickly, based on the subtle differences in the bumps on the inside of the brain—or we could fall into a modern-day neurological version of the trap that doctors of the 18th and 19th centuries fell into when they used facial features or bumps on the outside of the head to decide who had criminal tendencies or other unsavory moral characteristics (see Gould, 1981, for a historical perspective). To use a metaphor: If gardeners treated their flowers like psychiatrists do their “ADHD” patients, we might well hear things like “This lily has petal-deficit disorder!” or “My ivy has gone hyperactive!” We should consider the possibility that neurological diversity may be a potentially healthy development.
A third source of support for the belief that ADD/ADHD is a neurobiological disorder comes from genetic studies. In one study that received almost as much publicity as the 1990 Zametkin PET scan study described above (for an example of media attention, see Maugh, 1996), researchers at the University of California-Irvine claimed to have found a link between children with ADHD and a specific gene (the dopamine D4 receptor gene) associated with “novelty seeking” behavior (LaHoste et al., 1996).
An article that appeared in the same journal, Molecular Biology, a few months later (Malhatra et al., 1996), however, questioned whether there even was a link between the dopamine D4 receptor gene and the behavioral trait of novelty seeking in the first place. More recently, a follow-up article in Molecular Biology suggested that new data did not support an association between this gene and the brains of people identified as having ADHD (Castellanos et al., 1998).
In another study that garnered much publicity (“Hyperactive Behavior in English Schoolchildren,” by Taylor & Sandberg, 1984), researchers at NIMH claimed that some cases of ADHD were due to a thyroid disorder caused by mutations in a thyroid receptor gene (Hauser et al., 1993). A follow-up study among 132 children labeled with ADHD, however, revealed no evidence of clinically significant thyroid dysfunction (Spencer, Biederman, Wilens, & Guite, 1995).
Many difficulties are inherent in attempting to build a case for a genetic basis for ADHD. First, how can one reduce the complex feelings, behaviors, and thoughts of a person to a single gene (an “ADHD” gene) or even to a series of such genes? As Harvard Professor Emeritus of Biology Ruth Hubbard explains in relation to another common educational label, learning disabilities:
There is an enormous distance from a gene and the protein in whose synthesis it is implicated to a complex behavior like a “learning disability.” Psychologists and educators need to understand this and to stop expecting practical benefits from oversimplified correlations (Hubbard & Wald, 1993, p. 129).
Second, the traits associated with ADHD are quite generalized and may look very different in different contexts. The media have variously described the dopamine D4 receptor gene as a gene for “novelty-seeking,” “thrill-seeking,” or “risk-taking.” Each of these terms implies different things, some more positive than others. Risk-taking sounds dangerous. However, novelty-seeking may actually be a good thing. In fact, in research I describe in the next chapter, the traits of a creative person (including a penchant for novelty-seeking) look very much like the “symptoms” of ADHD. So perhaps that trait is heritable, though two studies suggest that it is not (Castellanos et al., 1998; LaHoste, 1996). But does that mean that something called “ADHD” is heritable? One must make a big leap of faith to make that connection.
Finally, genetic traits are not necessarily immutable factors hard-wired into our nature from conception on. Recent research suggests that the environment may have a much larger role to play in the modification of genetic material than previously thought possible. In one study at McGill University, researchers separated newborn rats from their mothers for either 15 minutes or six hours a day. One of the researchers, biologist Michael Meaney, reported: “We found that receptors [for certain brain chemicals] and the gene for the receptors are both altered” as a result of the stress of separation in the six-hour group (Begley, 1996, p. 57).
It is quite possible, then, that stress or other environmental influences can play a wide role in the disruption of the genetic blueprint for the flow of neurotransmitters in the brains of children labeled ADD/ADHD. In such a case, it becomes problematic to say that ADD/ADHD is purely a biological or medical disorder. At best, it is more likely an intricate dance between genetic predispositions and environmental events that trigger the symptoms associated with ADD/ADHD.
Again, ADD/ADHD looks much more like a complex interaction between brain and world than any kind of intrinsic medical problem located solely inside the genes or brain chemicals of a child. Unfortunately, our culture has tended to engage in wholesale “bioreductionism” of traits and characteristics once thought to be a natural part of the spectrum of human variation. One theoretical biologist, Brian Goodwin, suggests: “We need to develop a way of doing biology by going beyond the gene and cultivating intuitive ways of knowing about wholes and about organisms” (cited in Blakeslee, 1997). The biological should be an important part of a holistic approach to children labeled ADD/ADHD, but it should not take the central reductive role that it does in the current ADD/ADHD paradigm.
The existence of the symptoms of hyperactivity, distractibility, and impulsivity in schoolchildren is not merely a belief, it is an observed fact. To claim that these kinds of behavior represent the chief manifestations of something called ADD/ADHD, however, brings us into the realm of belief—a belief that can be questioned. This is particularly true because hyperactivity, distractibility, and impulsivity are among the most global and widespread types of behavior seen in childhood and adolescence. One can observe them in virtually all children during certain parts of their lives (especially in the early years and during adolescence), and under certain types of conditions at other stages of life that involve stress, boredom, excitement, and the like. A child can be hyperactive, distractible, or impulsive because she is depressed, anxious, allergic to milk, highly creative, bored with schoolwork, unable to read, or temperamentally difficult, among a host of other factors. How can we be precise in defining ADD/ADHD if we base identification—and labeling of children—on some combination of these three highly global kinds of behavior? What certainty exists here?
This matter is made even more uncertain when we look at studies suggesting that among children who are labeled ADD/ADHD, the symptoms of hyperactivity, distractibility, or impulsivity can decrease in intensity and even disappear in certain psychosocial contexts. Research suggests that ADD/ADHD-identified kids behave more normally in situations such as the following:
Consequently, the symptoms of ADD/ADHD appear to be highly context-specific. The vagueness of the behavioral criteria used to establish a diagnosis of ADD/ADHD has led to a growing literature critical of the ADD/ADHD paradigm (e.g., Armstrong, 1997; Goodman & Poillion, 1992; McGuiness, 1989; Reid, R., Maag, & Vasa, 1993). This fuzziness will become even more apparent when we examine the assessments used to diagnose ADD/ADHD.
The American Psychiatric Association (1994, p. 82), in its Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV), indicates that 3–5 percent of all schoolchildren have ADHD; and many sources on ADD/ADHD have followed this source (e.g., CH.A.D.D., 1994; Wallis, 1994). A wider review of the literature, however, will show quite a range of perceived variation in the incidence of ADD/ADHD. Here are some examples:
Barkley's comment is telling, because it suggests that the definition of ADHD is still highly unstable and depends to a good degree on the subjective decisions of a group of people who appear not to agree with each other on what constitutes genuine ADHD (McGuinness, 1989). At one time, clinicians in the United States and Britain considered the symptoms associated with ADHD to affect only a very small proportion of the total population (less than 1 percent) (see Goodman & Poillion, 1992; Taylor & Sandberg, 1984). The past few years, however, have seen a definite “drift” toward larger and larger percentages of incidence of ADHD. Most recently, Ratey and Johnson (1998) have suggested that there may be a subclinical variety of ADHD that could extend the ADHD net over an even wider population. That ADHD should be seen as residing in a substantial proportion of the population (say, over 10 percent) when 20 years ago its existence was virtually unknown should give us pause. Could it be that the ADD/ADHD paradigm is transforming aspects of behavior that were once considered a normal part of human variation into pathological aberrations? If so, what impact is this creeping medicalization of human behavior likely to have in other spheres? Could we soon see other aspects of human variation turned into disorders (e.g., courage-deficit disorder, truth-deficit disorder, ambition-deficit disorder)?
As suggested in the previous section, the variation in the numbers of people suspected of having ADD/ADHD appears to be directly related to problems with the assessments used to diagnose it. As the DSM-IV indicates: “There are no laboratory tests that have been established as diagnostic in the clinical assessment of Attention-Deficit/Hyperactivity Disorder” (American Psychiatric Association, 1994, p. 81). Consequently, professionals have had to make do with a number of methods and instruments that have had significant reliability and validity problems.
What would seem to be one of the most solid approaches—an office visit to and interview with a physician trained to diagnose ADHD—appears to be one of the least successful approaches (except to rule out other possible medical problems) because research suggests that 80 percent of the time the symptoms of ADHD “disappear” in the doctor's office (Sleator & Ullmann, 1981). Reasons for this include the one-to-one relationship with a (usually) male authority in a novel environment (all factors that, as discussed in the previous section, reduce or eliminate the symptoms associated with ADD/ADHD). As a result, the assessment mainstays of ADD/ADHD diagnoses have tended to turn on two major sources of information: observations/rating scales, continuous performance tasks, and psychological testing.
Behavior rating scales are typically checklists consisting of items that relate to a child's attention and behavior at home and school. In one widely used scale, teachers are asked to rate the child on a scale of 1 (almost never) to 5 (almost always) in terms of behavioral statements such as “Fidgety (hands always busy),” “Restless (squirms in seat),” and “Follows a sequence of instructions.”
The main difficulty with these sorts of instruments is that they rest entirely on subjective judgments. How is a teacher to score a child, for example, on “Restless (squirms in seat)”? Perhaps the child squirms when required to take tests or do worksheets, but possibly not when involved in a hands-on activity. There is no room for this kind of distinction on the rating scale. Moreover, there are value judgments attached to a statement like “squirms in seat.” The implication seems to be that squirming is a bad thing (e.g., leading toward a diagnosis of ADHD). But what if the child squirms due to excitement and anticipation in learning something new, or as a natural part of a highly physical nature? Moreover, whereas scales like these are focused on identifying, for example, hyperactivity, there should statistically speaking also be another pole on that axis that points to hypoactivity (the underactive child). And yet one never sees scales to identify and treat the hypoactive child. The inherent problems involved in constructing a valid scale may help explain why these scales often involve such poor agreement between groups who fill them out (McGuiness, 1985, 1989; Reid, R., & Magg, 1994).
Continuous performance tasks (CPT) appear to have resolved the problem of rating scale subjectivity by turning the assessment over to a machine (usually computerized). These tasks involve repetitive actions that require the child to remain alert and attentive throughout the test. The earliest versions of these tasks were developed to select candidates for radar operations during World War II. Their relevance to the lives of today's children seems highly tenuous.
One popular CPT instrument consists of a plastic box with a large button on the front and an electronic display above it that flashes a series of random digits. The child is told to press the button every time a “1” is followed by a “9.” The box then records the number of “hits” and “misses” made by the child. Quite apart from the fact that this task bears no resemblance to anything else that the child will ever do in his life, this instrument creates an “objective” score that is taken as an important measure of his likelihood of having ADHD. Most recently, it has been used in functional magnetic resonance imaging (fMRI) studies to show differences in brain activity between children labeled ADHD and those identified as normal (Vaidya et al., 1998). In reality, it only tells us how a child will perform when forced to attend to a series of meaningless numbers on an Orwellian machine.
These types of decontextualized assessments attempt to make judgments about the whole child in terms of a tiny fraction of split-off moments of artificial experience in the life of a human being. As such, their validity—in the broadest possible sense of that word—remains highly problematic.
Educators and psychologists have used other standardized diagnostic instruments in an attempt to discriminate ADD/ADHD from non-ADD/ADHD groups, including the following:
Yet even prominent figures in the ADD/ADHD world believe that such measures are misleading (e.g., Barkley, 1990, pp. 330–332).
Research strongly supports the effectiveness of medications such as methyphenidate hydrochloride (Ritalin) on a range of outcomes, including reduction of large and small motor movements and increased attentiveness, especially in structured, task-oriented settings such as traditional classrooms (Abikoff & Gittelman, 1985). The medication is also associated with improvements in compliance with teacher or parent directives; reduction of aggressiveness with peers; and improved social relationships with parents, teachers, and peers (Swanson et al., 1993). If the meaning of “effective” is related to these types of outwardly observable behavioral changes, then this assumption of the ADD/ADHD paradigm could be seen as correct.
Some inherent problems with Ritalin use, however, may limit its true “effectiveness” in any deeper sense of that word. As Swanson and colleagues (1993) point out, the benefits of stimulant medications are temporary. Ritalin, for example, is a short-acting drug whose effects wear off after a few hours. Consequently, it is not by any means a “cure” or even a serious attempt to get at the root of whatever ADD/ADHD may turn out to be. It simply provides symptomatic relief.
One of the biggest problems with Ritalin is that it works so effectively. Because it quells a child's hyperactivity, impulsivity, or distractibility, parents, teachers, and professionals may be lulled into a feeling that the problem has been solved. This may keep them from attempting to use nonmedical approaches that might actually go much more deeply into the core of a child's behavioral or attentional difficulties (e.g., emotional distress, learning problems).
Ritalin also has some specific drawbacks, which many writers on the subject of ADD/ADHD have ignored or downplayed. Here are several of these disadvantages:
Ritalin clearly has its place in any holistic model of attention and behavior difficulties (American Academy of Pediatrics, 1987; Turecki, 1989, p. 231). In such a context, it would appear to be a powerful tool to treat aspects of the child's difficulties that stem from biological roots.
The model I am proposing in this book, however, does not consider the biological to be the central core of the “problem” (at least for many kids labeled ADD/ADHD), but one of its many “hubs” (see Chapter 2). Thus I maintain that educators should not consider Ritalin use (and the use of other psychoactive drugs) as “the first and most effective treatment,” but as one among a wide range of possible tools that educators and parents can use to help children with attention and behavioral difficulties. The difficulty with Ritalin is not that children take it, but that many professionals and parents turn to it too quickly and advocate its use with too many kids who may not actually need it when provided with access to a broader range of strategies (see Breggin, 1998; Diller, 1998; Divoky, 1989; Garber, Garber, & Spizman, 1997).
According to ADD/ADHD texts, people used to think that the symptoms associated with ADD/ADHD disappeared after childhood. However, research now suggests that some kids labeled ADD/ADHD will continue to have the “disorder” into adolescence and adulthood (American Psychiatric Association, 1994; Klein & Mannuzza, 1991). These findings have fueled a new growth industry in ADD/ADHD even greater than that originally developed around children: one geared toward the needs of the “ADD/ADHD adult” (Sudderth & Kandel, 1997).
What's missing from discussions of this new research, however, is the obvious complement to these findings: If some kids labeled ADD/ADHD will continue to have ADD/ADHD into adulthood, it logically follows that for some kids identified as ADD/ADHD the disorder will disappear! As the DSM-IV points out:
In most individuals, symptoms attenuate during late adolescence and adulthood, although a minority experience the full complement of symptoms of Attention-Deficit/Hyperactivity Disorder into mid-adulthood. Other adults may retain only some of the symptoms, in which case the diagnosis of Attention-Deficit/Hyperactivity Disorder, In Partial Remission, should be used (American sychiatric Association, 1994, p. 82).
When this type of argument is posed, however, we seem to move out of the biological paradigm—on which ADD/ADHD is based—and into a more developmental paradigm, which has different assumptions about learning and growth from those espoused by ADD/ADHD adherents (see the next chapter for a fuller discussion of a developmental perspective). Although one certainly might argue that “many children with ADD/ADHD learn to compensate for their symptoms in adulthood,” one might also argue the flip side, that “people with hyperactive behavior in childhood mature and discover the value of their hyperactivity in adulthood and learn to use it to better their lives and the lives of others.”
In the ADD/ADHD “half-empty glass” approach, the disorder remains into adulthood but is “minimal” or “in remission.” In the more holistic/developmental “half-full glass” approach, the person grows up and, in maturing, may in fact discover that the very things that gave her so much trouble in childhood were the same traits that ultimately led to her success in adulthood!
This assumption that a child can have ADD/ADHD along with disorders like learning disabilities and anxiety or mood disorders includes an assumption that there are different subtypes of ADD/ADHD. This last assumption of the ADD/ADHD paradigm is the most tricky one.
As discussed earlier in this chapter, there are many problems with the definition of ADD/ADHD. As the next chapter shows, researchers have discovered many other ways of explaining hyperactivity, impulsivity, and distractibility, than by positing the existence of a discrete disorder such as ADD/ADHD. For example, the next chapter discusses how a child can be hyperactive because he is anxious or depressed, or is frustrated in learning at home and school.
How can one be certain that the hyperactivity doesn't stem from these deeper problems? ADD/ADHD experts have found a way to preserve their disorder (and thus, the entire paradigm) while explaining these anomalies at the same time. “It's simple,” they might argue. “A child can be both ADD/ADHD and have an anxiety disorder [or a mood disorder, or a learning disability].” This sort of multiple-disorder approach is referred to as “comorbidity.” Such reasoning begs the question of where the attention-deficit disorder leaves off and the anxiety disorder or learning disability begins. It allows the ADD/ADHD exponents to avoid the sticky problem of “confounding variables” (e.g., “We're not sure if it's anxiety or ADD/ADHD, so let's just say that it's both”).
The same type of fractional approach has been used to deal with anomalies observed in children labeled ADD/ADHD that don't seem to fit into the original definition of an “attention deficit.” For example, some parents might argue “But my child doesn't have trouble paying attention; in fact, he'll spend hours working on his Legos [or playing video games, or participating in other activities he enjoys].”
Instead of regarding this as an anomaly that challenges the foundations of the ADD/ADHD paradigm, ADD/ADHD researchers simply adjust the paradigms lightly to accommodate these new findings. “You see,” they might explain to the parent, “we now know that this sort of behavior is part of the problem—we're calling it hyper-focus, and it's something that we're seeing in an increasing percentage of ADD/ADHD kids.”
The very dual nature of the term itself—ADD/ADHD—reveals an attempt to cope with the observation that some kids once thought to be ADD were hyperactive, and other kids were not at all, but more distractible. Instead of using this as an opportunity to rethink the whole paradigm, the response was to retain the paradigm and simply to begin speaking of “subtypes.” The proliferation of “comorbid” factors and subtypes in the ADD/ADHD world (American Psychiatric Association, 1994; Biederman, Newcorn, & Sprich, 1991; Hallowell & Ratey, 1994a, 1994b) reveals the (so far successful) attempt by ADD/ADHD proponents to preserve the paradigm in the face of growing evidence that there are many kids who simply don't fit neatly into its structure.
A paradigm can accomplish this sort of thing for only so long before it begins to break up. The 2nd century C. E. astronomer Ptolemy, for example, kept adding little epicycles to his paradigm to account for anomalies in the supposedly circular motion of the planets. Finally, the 17th century scientist Johannes Kepler accounted for the anomalies by regarding the motion of the planets as ellipses. By taking a fundamentally different perspective on looking at the motion of planets (or shifting the paradigm), Kepler was able to better account for the astronomical data then available to scientists. In the same manner, the ADD/ADHD world has attempted to account for the increasing number of anomalies in its paradigm by adding its own version of “epicycles” (e.g., subtypes, comorbid factors).
A holistic approach to the ADD/ADHD issue seeks to do away with this “add-on-the-categories” method of accounting for anomalies, and instead looks for a better way to make sense of the great diversity among kids who experience attention and behavior difficulties in the classroom. Chapter 2 explores a number of alternative paradigms or perspectives that attempt to explain this diversity in a richer way.
Copyright © 1999 by Thomas Armstrong. All rights reserved.
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