Attention Deficit / Hyperactivity Disorder
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Asperger’s in Adults: You think you know the faces of Asperger’s Autism
Transcription
2:30
Some people have argued ADHD is merely a social construct with the division between “normal”
2:35
and “abnormal” completely arbitrary. By using real-life impairment resulting from
2:39
the symptoms, the diagnosis can be made less subjective and arbitrary.
2:43
ADHD is identified and diagnosed by its symptoms. It is generally agreed that these symptoms
2:48
result from one or more neurological deficiencies, but the specific deficiencies and the best
2:52
way to treat them are areas of hot debate and active research. The primary theories
2:57
are: (1) dopamine deficiencies, (2) low arousal to external stimuli, and (3) working memory
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deficits. Dopamine is a neurotransmitter that controls
3:05
the flow of information coming from other parts of the brain. By emphasizing important
3:10
stimuli and suppressing others, it functions like a traffic light for incoming information.
3:14
Hypodopaminergia has also been implicated as a possible cause for deficits in executive
3:19
functioning which is responsible for planning, initiating and inhibiting actions, and selecting
3:24
relevant sensory data. The high effectiveness of stimulants with dopaminergic effects as
3:28
treatment for ADHD in double-blind controlled trials has supported this theory for over
3:33
30 years. According to the low arousal theory, people
3:36
with ADHD react less to external stimuli than people without the disorder. In order to maintain
3:42
the level of mental arousal necessary to be focused and attentive, a person with ADHD
3:46
will try to generate additional stimulation by walking around, fidgeting, talking, or
3:50
bouncing in their chair. This theory has been supported twofold: first, by the effectiveness
3:55
of stimulants independent of dopaminergic effects. Both methylphenidate and caffeine
4:00
have proven effective in low doses at increasing mental arousal and decreasing hyperactive
4:04
and inattentive behavior. Additionally, the use of bright colors to emphasize tasks has
4:09
been shown to be highly effective at drawing and maintaining attention towards the current
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task and increasing overall performance, even when the added color had no relation to the
4:17
specific task. Recent studies have shown a statistically
4:20
significant correlation between demands on working memory and hyperactive behavior. An
4:25
extension of the low arousal theory, the working memory model suggests that hyperactive behavior
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is a direct result of increased demands on working memory, and that the hyperactive behavior
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consistently ceases immediately following a decrease in working memory demand.
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In addition to the uncertainty about which deficits cause ADHD, the causes for the proposed
4:43
deficits are unknown and also under active research. Current theories can be separated
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into two basic categories: environmental and genetic. Research studies have shown that
4:53
ADHD may be caused by toxins introduced during pregnancy and early development, such as alcohol,
4:57
tobacco, lead, and certain insecticides. Premature birth and certain artificial food colorings
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have also been correlated with ADHD. In the genetic category, multiple twin studies have
5:08
indicated that the disease is highly heritable and that genetics are a factor in 75% of all
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cases. In a recent study of over 30,000 patients, subjects with ADHD were significantly more
5:19
likely than controls to have large, rare chromosomal structure abnormalities that have previously
5:24
been associated with other neurodevelopmental disorders including intellectual disability,
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schizophrenia, and autism. Although it is safe to assume that genes play a role in ADHD
5:34
and its heritability, ADHD is best understood as the result of a complex interaction of
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genetic and environmental factors that are not yet clearly understood.
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Although some DSM-IV recognized disorders can be maintained through external influences
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or behavioral patterns, given that symptoms of ADHD are caused by neurological differences,
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ADHD is considered to be an incurable, but manageable, disorder.
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As a result of the wide variety of possible deficiencies and resulting symptoms, treatment
6:01
for ADHD is usually planned on a very individualized basis to address the patient’s specific
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symptoms and deficiencies. The most effective and most commonly used treatment plan is a
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combination of medication and behavioral therapy. The most commonly used medications for treatment
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of ADHD are stimulants with dopaminergic effects, such as methylphenidate and dextroamphetamine,
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commonly known as Ritalin and Adderall, respectively. These drugs are believed to reduce ADHD symptoms
6:27
by increasing dopamine thereby allowing the brain to self-regulate incoming stimuli. Another
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recently released medication is atomoxetine, marketed as Strattera, which is a selective
6:38
norepinephrine reuptake inhibitor. Originally intended as an antidepressant, atomoxetine
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has been highly effective at treating ADHD without the withdrawal and abuse risks associated
6:49
with stimulants. In addition to medication, most psychologists
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recommend behavioral therapy to provide special attention to areas where people with ADHD
6:57
generally struggle. These include organization and management of time, tasks, and distractions.
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The most commonly taught skills are using a calendar and task list, breaking down overwhelming
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tasks into smaller steps, and writing down distractions for later instead of acting on
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them write away. In addition to therapy for the patient, education is generally recommended
7:17
for parents and teachers who will be working with the patient. This generally involves
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instruction about ADHD and suggests certain techniques like highlighting that have proven
7:25
to be very effective when teaching people with ADHD. In addition to these basic skills,
7:30
therapy sessions are usually specifically tailored to a patient’s needs.
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Due to the high incidence rate of ADHD and enhanced creativity, some have chosen to regard
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ADHD as a “difference” rather than a “disorder.” They argue that perceived impairment is due
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to the strict academic mold posed in the modern education system: students with ADHD think
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and learn differently from the way they are taught and tested, resulting in significant
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academic difficulties. This also explains the perception that children grow out of their
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ADHD or it just goes away when they complete their formal education: instead of ADHD going
8:04
away, the release from a specific learning and knowledge application process allows the
8:08
child to learn and work in a way that their ADHD symptoms do not cause impairment. Some
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have even extended this farther to claim that ADHD is a gift because an inability to focus
8:18
solely on a single idea can enable thinking outside the box and result in new and unique
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solutions to a problem. While it is difficult to say anything definitive
8:27
about ADHD due to the many uncertainties about the neurological and underlying causes, research
8:32
and debate over ADHD will likely continue for many years as scientists continue to learn
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more about the true final frontier: the human brain.