Discussion
In the school’s psychoeducational evaluation, reports from Michael’s teachers showed clinically significant symptoms of attention deficit hyperactivity disorder (ADHD), and the parents’ reports showed mildly elevated risk in the clinical range of ADHD. Michael’s mother—who, when Michael’s history was being taken, mentioned that she often wondered if her husband “had a touch of ADHD”—rated Michael’s behaviors at a higher level of risk than his father’s. One of the keys in diagnosing ADHD is that the symptoms are present both at school and at home. This is important, as a diagnosis of ADHD requires that the behavior must occur both at home and at school.
Michael’s math and reading teachers also ranked his difficulties in these subjects as consistent with symptoms of ADHD. The Woodcock-Johnson Test of Academic Achievement indicated that Michael was in the 37th percentile for reading and mathematics. Although these scores were lower than average, they were within the expected range of functioning, given his IQ score of 102. Many children with ADHD have above-average IQ scores. Also, when provided with academic curricular tests in a 1:1 environment with focusing cues and no distractions, Michael did better on the tests than he did when they were administered in a classroom environment with distractions and time constraints.
Treatment recommendations included a family education program on how to best structure Michael's home schedule and initiation of a stimulant medication by the referring pediatrician.[1]
With regard to a biologic explanation for ADHD, abnormal activity of the neurotransmitter dopamine—including lower dopamine activity in the limbic system, as revealed on positron emission tomography (PET) scans—has been noted in some persons with ADHD.[2,3] These changes in dopamine activity may explain why medications that act to increase dopamine, such as methylphenidate, have been effective in treating ADHD.[4] Research indicates that dysregulation and changes in the activity of the neurotransmitter norepinephrine are also associated with ADHD. The lower levels of the neurotransmitters (dopamine and norepinephrine) in patients with ADHD helps explain the paradox of providing treatment that includes a stimulant, such as methylphenidate, to persons who are already hyperactive.
Evidence has also demonstrated frontostriatal malfunctioning in ADHD,[5] and research has demonstrated the existence of deformations in the basal ganglia (caudate, putamen, globus pallidus) that are normalized by stimulant medications.[6] Another clue to the biologic etiology of ADHD is evidence that it is genetically transmissible.[7] In the case of Michael, for example, his father may have it.
In addition to biologic factors, ADHD can be affected by environmental and sociologic ones as well; specifically, stress and labeling. Conflicts, pressure, family dysfunction, and the mere phenomenon of being labeled as having ADHD may exacerbate current symptoms of the condition and produce other symptoms of ADHD that were not initially present.[2]
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Cite this: A 12-Year-Old Boy With Falling Grades and Forgetful Behavior - Medscape - Jun 25, 2019.
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