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ADHD is characterized by inattention, hyperactivity, and impulsivity excessive for the age or developmental level. Standard diagnosis specifies that by the time a child reaches seven years, at least six of the features listed below under "inattention," plus a combined total of at least six of the items listed under "hyperactivity" and "impulsivity," must all be present.
(a) won't pay attention to details, makes many careless mistakes in schoolwork or other chores;
(b) can't sustain attention in tasks or games;
(c) seems not to listen properly when spoken to;
(d) doesn't follow instructions well, and often fails to complete tasks;
(e) has a hard time organizing tasks;
(f) has a hard time with activities or tasks that require a sustained mental effort;
(g) frequently loses things needed for tasks or activities, such as pencils, books, toys;
(h) is easily distracted;
(i) is often forgetful in routine activities.
(a) fidgets or squirms excessively;
(b) leaves seat when sitting is required;
(c) runs around or climbs on things excessively;
(d) has a hard time with quiet activities;
(e) seems to be in constant motion;
(f) talks excessively.
(a) blurts out answers before the question has even been finished;
(b) has a hard time waiting to take turn;
(c) interrupts or butts in on others.
Attention-Deficit/ Hyperactivity Disorder
Attention-Deficit/ Hyperactivity Disorder, or ADHD, is one of the most common- disorders included in this book. It is generally accepted that about three to five percent of school-age children have it, although some place the rate of occurrence as high as 24 percent. And yet twenty years ago nobody had even heard of the disorder. Have children suddenly become less attentive and more hyperactive?
Probably not. The dramatic increase in ADHD diagnoses is more the result of a heightened awareness of the disorder and the passage of laws requiring public schools to identify and help students who have it. Largely because of this new legislation, outpatient visits for ADHD almost tripled from 1990 to 1993 alone.
The reason, then, that ADHD has become so commonplace is the same reason so many more people suddenly seemed to suffer from low-level depression: behavior that used to be viewed as a sign of weak character is now understood to result from a brain-based imbalance.
In the case of depression, common-enough human feelings such as low self-esteem, pessimism, and passivity are now considered to be linked to low levels of serotonin in the brain, and are treated with drugs of the Prozac class that work by raising levels of that neurotransmitter. By an interesting kind of logic, the very fact that certain temperamental traits can be "cured" on a biochemical level by medication means that people who respond well to such medicine are now understood to be ill, rather than "lazy," or "weak," or "just a little different."
In the case of ADHD, the most widespread current opinion is that this disorder also stems from a neurotransmitter imbalance. According to many researchers, the neurotransmitter implicated in ADHD is dopamine, and something about the brain of someone with ADHD results in dopamine levels being too high. This in turn results in behavior that is, in some ways, the opposite of the dour, stiff, stoic, and eventually physically frozen behavior of someone with a dopamine- deficiency disease like Parkinson's.
One of the reasons the symptoms of ADHD haven't traditionally been taken seriously is that they are, in many ways, exaggerated versions of the kind of behavioral traits that small children typically exhibit anyway — inattentiveness, hyperactivity, and low impulse control. The difference between a child with ADHD and those without it lies in both the severity of the symptoms — especially in children of early school age — and in the delay in outgrowing the inattentive, hyperactive, and impulsive behavior as quickly as other children.
Because children are expected to learn to have more focus and self-control simply in the process of "growing up," older children with ADHD are often treated with disapproval by adults — which only worsens another symptom of ADHD, an acute sense of low self-esteem.
In fact, it makes about as much sense to criticize an ADHD child for being lazy or contrary-minded as it would be to criticize any small child for telling falsehoods in response to the suggestions of an adult. One of the reasons young children's testimony in cases of alleged preschool abuse is viewed so cautiously is that their brains (more specifically, their frontal lobes) simply haven't developed sufficiently to keep careful track of where an idea came from — whether from actual first-hand experience or in response to the suggestion of a well-meaning adult. An understanding of this will help us avoid blaming young children if what they say turns out to be wrong. It's not that they're really lying —it's just that their frontal lobes haven't developed enough to give them the kind of "source memory" that most adults have.
What causes ADHD?
One of the keys to understanding ADHD, as suggested earlier, may lie in the frontal lobes. The front part of the brain houses regions responsible for "executive-attention" skills — monitoring and regulating one's own behavior, controlling one's emotions, taking the necessary steps to achieve goals, and so on. An imbalance occurs in ADHD between the input of the still immature centers in the right hemisphere (anterior cingulate) that focus attention and the prefrontal area that selects goals and predicts how to reach them. (Some research also shows immaturity in another area, near the hearing centers, that coordinates various and varied incoming data into the meaningful "big picture.") Young children, and adults with frontal lobe injury, often lack focus and planning skills, and may seem irresponsible and sometimes even antisocial as a result.
ADHD in adults
While many people have heard about ADHD in children, it is also a problem that may affect as much as 2% of the adult population. Adult symptoms include low tolerance for frustration or delay (waiting in line or in traffic can be a major ordeal for ADHD adults), and, in social situations, conduct that could be described as intrusive, gregarious, and over-talkative — the adult version of the class clown. Nonetheless, it is important to remember that ADHD diagnosis in adults is even more difficult to define than it is in children, especially in this caffeine-charged age of digitized information and instant gratification — a time when it seems as if the whole society has a touch of ADHD.
Why would young children lack frontal-lobe-based skills?
To answer this question, it's necessary to correct a common misconception that the quality and quantity of our brain cells are at their peak when we're born, and that things just go downhill from there. In fact, a lot of brain development happens well after birth. The frontal lobes are, in evolutionary terms, the most recently-developed part of our brain. That means that they're also one of the slowest parts to develop as our brain grows and matures. Some researchers believe that the full development of the brain's frontal cortex isn't complete until the mid-twenties, or even later.
Working Memory Span
Children with ADHD tend to perform poorly on "executive-control" tasks such as tests of working memory — the kind of short-term memory that allows you to retain information while you're monitoring, judging, or manipulating it "on- line." Amphetamine medication tends to increase attention span and improve working memory tasks.
One test of working memory is called the Working Memory Span. For this test, read each of the three sentences in each set out loud to someone and ask her to tell you immediately after you read each sentence whether it is absurd or makes sense. After each set, ask the person to name the objects (car, sky, etc.) mentioned in the three sentences.
|Set 1||Set 2|
|The mechanic fixed the car.
The waitress fed the sky.
The gardener watered the plants.
|The boy walked the piano.
The teacher graded the test.
The man drove the grass.
An Unsettling Discovery
Very recently researchers at the University of Pittsburgh discovered a high correlation between children with lead poisoning (a high level of lead deposits in their bones) and children convicted for legally delinquent behavior. Lead poisoning causes damage to the prefrontal lobes. New research is now under way there to investigate whether a similar correlation exists for children diagnosed as having Attention Deficit Disorder.
Since the frontal lobes are developing through adolescence even in ADHD children, symptoms of the disorder tend to lessen with age. By early adolescence, a frantic inability to remain seated is often replaced by mere restlessness or fidgetiness, and by early adulthood the fidgetiness may turn into a mere dislike of sedentary activities and a preference for employment and hobbies that permit free and frequent movement. However, symptoms of inattention (for example, difficulty organizing tasks requiring working memory and sustaining effort and attention until completing them) tend not to lessen as much. In about one third of people diagnosed with ADHD in childhood, the symptoms are reduced enough by adolescence that they're no longer considered to have the disorder. The percentage climbs to about 70 by adulthood.
This typical progression of ADHD makes this brain disorder different from many others, such as mood disorders (depression or bipolar disorder, for example) and anxiety disorders. Mood and anxiety disorders may also feature symptoms of inattention but tend to appear only after age seven, and tend to become more severe with age.
What about the role of the neurotransmitter dopamine?
Dopamine is known to be centrally involved in reward-seeking and novelty-seeking behavior, and in the motivation to use and move one's body. As already mentioned, when Parkinson's patients lose the ability to produce dopamine, they become dour, stoic, and, eventually, paralyzed. In many ways, ADHD seems just the opposite of this. So it stands to reason that ADHD symptoms might be related to an excess of dopamine. Support for a role of dopamine in ADHD comes from the seemingly paradoxical success of stimulant drugs (of which Ritalin is one brand name) in alleviating the symptoms of the disorder. The effect of these stimulants seems to be to block the reabsorption of dopamine back into the transmitting brain cell, thereby increasing dopamine levels in the synapse.
The puzzling question this prompts is, if ADHD symptoms result from an excess of dopamine, why would increasing their levels serve to relieve these symptoms?
Perhaps it isn't really too much dopamine that people with ADHD suffer from. One recent study indicates that ADHD patients actually have an increase in the dopamine transporter molecule, which reduces dopamine levels by taking the neurotransmitter back up into the transmitting cell. In that case, though, why is it that ADHD symptoms are essentially the opposite of those of Parkinson's (a dopamine-deficiency disease) and similar to the dopamine- increasing effects of amphetamines?
The answer may lie in findings recently presented by a team of Duke University researchers. By breeding mice lacking the gene for the dopamine transporter ("DAT-knockout" mice), the researchers were able to experiment with animals that showed hyperactive and inattentive behavior that paralleled the behavior of a human with ADHD. The DAT-knockout mice also showed the same paradoxical response to amphetamines as people with ADHD: the treated mice actually calmed down, and performed better on maze-running tests.
Upon close examination of dopamine concentrations in the brains of the DAT- knockout mice, the research team determined that amphetamines that raised dopamine levels in normal mice had no effect on dopamine levels in the DAT- knockout mice. In other words, even though the hyperactive, inattentive behavior of these mice may have been due to excess dopamine, the calming effect of amphetamines couldn't have been due to any effect on dopamine levels, since those levels remained unchanged.
What, then, accounts for the calming effect of amphetamines?
Amphetamines don't just affect dopamine levels, but also raise levels of other neurotransmitters, including serotonin. Serotonin is the neurotransmitter that is raised by drugs such as Prozac. It is considered a "calming" neurotransmitter, conducive to mental focus and well-being. The researchers gave a variety of serotonin-specific drugs to the mice — that is, drugs that raise levels of serotonin but not of any other neurotransmitter — and found that their behavior and learning curves improved just as if they had been given amphetamines. The serotonin-increasing drugs had no effect on the behavior or performance of normal mice. Thus, according to this evidence, it is a rise in serotonin levels, rather than an increase or decrease in dopamine, that accounts for the beneficial effect of the amphetamines.
A new treatment for ADHD?
These findings have important implications for the treatment of ADHD in humans. Even though children with ADHD have been treated with amphetamines since the 1930s, this kind of treatment has always been controversial. Among other things, there is evidence that amphetamines are "neurotoxic" — harmful to brain cells. If raising serotonin levels relieves ADHD symptoms, then serotonin-selective drugs may be just as helpful in treating these symptoms without any of the harmful side-effects of amphetamines.
Prescribing psychotropic drugs for preschoolers
Parents and teachers well know that the normal behavior of preschoolers often looks a lot like ADHD. A recent survey of state Medicaid programs in the Northwest revealed that the use of stimulants normally prescribed to treat ADHD — most commonly methylphenidate, the generic form of Ritalin — recently increased two- and sometimes threefold for children under four years old. Though such medications are effective for ADHD, an author of that study was doubtful that preschoolers could meet the diagnostic criteria for either ADHD or depression — the probable diagnoses given to justify the prescribed medications.
Where to learn more:
American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders: DSM-IV. Washington, DC: American Psychiatric Association.
Baddeley, A. (1998) "Recent developments in working memory." Current Opinion in Neurobiology 8, 234-238
A. Berger and M.I. Posner (2000). "Pathologies of brain attentional networks." Neuroscience and Biobehavioral Reviews 24: 3-5.
Darin D. Dougherty et al. (1999). "Dopamine transporter density in patients with attention deficit hyperactivity disorder." The Lancet 351: 2132-3.
Harvard Health Letter 25/5: 4-5.
Raul R. Gainetdinov et al. (1999). "Role of serotonin in the paradoxical calming effect of psychostimulants on hyperactivity." Science 283: 397-401.
K. Rubia et al. (2000). "Functional frontalisation with age: mapping neurodevelopmental trajectories with fMRI." Neuroscience and Biobehavioral Reviews 24: 13-19.
J.M. Swanson et al. (2000). "Dopamine genes and ADHD." Neuroscience and Biobehavioral Reviews 24: 21-25.
J.M. Swanson et al. (1998). "Attention-deficit hyperactivity disorder and hyperkinetic disorder." The Lancet 351: 429-33.
J.M. Swanson, M. Lerner, and L. Williams (1995). "More frequent diagnosis of attention deficit-hyperactivity disorder." The New England Journal of Medicine 333: 944.
R. Tannock, A. Ickowiz, and R. Schachar (1995). "Differential effects of methylphenidate on working memory in ADHD children with and without comorbid anxiety." Journal of the American Academy of Child and Adolescent Psychiatry 34: 886-96.
Daniela Vallone, Roberto Picetti, and Emiliana Borrelli (2000). "Structure and function of dopamine receptors." Neuroscience and Biobehavioral Reviews 24: 125-32.
Julie Mango Zito et al (2000). "Trends in the prescribing of psychotropic medications to preschoolers." Journal of the American Medical Association 283/8: 1025-30.
Excerpted from Brains That Work a Little Bit Differently by Allen D. Bragdon and David Gamon. Copyright © 2000 by Allen D. Bragdon Publishers, Inc.. Excerpted by permission. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
|ADHD: Attention deficit and hyperactivity||9|
|ALCOHOLISM: Triggering transmitters||21|
|AUTISM: A mind unaware of itself and others||35|
|DÉJÀ VU: True hallucinations||49|
|DYSLEXIA: An island of disability within an ocean of|
|HANDEDNESS: Left turn signals||71|
|PERFECT PITCH: Tuned in the genes||79|
|PHOTOGRAPHIC MEMORY: Data, data everywhere||87|
|SEASONAL AFFECTIVE DISORDER: The winter blues||103|
|SYNESTHESIA: When the notes have coolors and letters make|
Posted April 22, 2008
We have been walking the special needs road for many years. While a lot of the information wasn't overwhelmingly new, it was nice to read it packaged in a relatively easy, quick-read format. If you are interested in the workings of the brain, this is a great read for those with a new and intermediate interest.Was this review helpful? Yes NoThank you for your feedback. Report this reviewThank you, this review has been flagged.