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May 30, 2001 6 min read
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Your article “Paying Attention: Scientists Scrutinize the Brain for Biological Clues to the Mysteries of adhd” (On Assignment, Research, May 9, 2001) could have benefited from a more balanced approach on the question of the biological origins of attention deficit hyperactivity disorder.

First, brain-imaging studies are still in their infancy, and the question of their diagnostic power is still in doubt. A recent review of brain-imaging studies appearing in the July 2000 issue of the Journal of the American Academy of Child and Adolescent Psychiatry suggests problems with these studies, including relatively small and often heterogeneous samples and difficulties in establishing accurate and appropriate diagnoses.

Second, the question of interpreting results should have been raised in the article. As the neurosurgeon Karl Pribram suggested in a workshop at a “Brain and Learning” conference May 4 in Washington, neuro-imaging studies such as are used in the field of ADHD may show correlations, but these do not necessarily translate to causation. In other words, the fact that brain-flow patterns are indicated in a scan does not mean that those areas of the brain are “causing” the behaviors of ADHD.

Third, there is the matter of modifiability. The implication from your article is that the brain patterns of so-called ADHD individuals are hard-wired in, and thus become an ineffable biological fingerprint of their ADHD status. However, other studies have suggested that it is possible to change one’s brain- scan images through specific environmental interventions (see, for example, “Systematic Changes in Cerebral Glucose Metabolic Rate After Successful Behavior Modification Treatment of Obsessive-Compulsive Disorder,” Archives of General Psychiatry, February 1996). Moreover, there are suggestions that environmental conditions such as stress may negatively affect neurological patterns, including prefrontal cortical function (Journal of the American Academy of Child and Adolescent Psychiatry, February 1999). Consequently, many kids labeled as having ADHD who show prefrontal abnormalities may have developed them as a result of lack of “nurture,” rather than a faulty “nature.”

Finally, there is the question of differences vs. disorders. The implication throughout your article is that we are tracking a biological disorder, and yet the brain-scan images that actually appear in the companion article (“Brains Doing Math Add to Knowledge of ADHD”) seem to suggest more of a cognitive difference than a disability. The individuals labeled as having ADHD showed more posterior activity (related to visual- spatial processing) than so-called normals. They pictured images in their heads. In other words, these scans may not be diagnosing ADHD as much as they are identifying individuals who process information through pictures and images more than through sounds and words; individuals who might be expected to have more difficulty in classroom environments where sounds and words predominate, and little use is made of visualization as a teaching technique.

One last quibble with the article is the uncritical acceptance of a genetic origin for ADHD. James Swanson did indeed have an article in the January 1998 issue of Molecular Psychiatry suggesting an association between ADHD and a defective gene for the D4 dopamine receptor. However, another article appeared later in the year in the same journal (September 1998) by Dr. Xavier Castellanos entitled, “Lack of an Association Between a Dopamine-4 Receptor Polymorphism and Attention-Deficit/Hyperactivity Disorder.” So there is controversy in the field, and your article should have reflected this.

The reason I am so concerned about raising these issues is that so many educators these days are too quick to regard students labeled as having ADHD as biologically defective, and this article simply gives them more fuel for their defective views of these kids. In fact, when one inquires more deeply into this subject, one discovers all sorts of intriguing, subtle, and compelling arguments against a purely biological description of the kinds of behaviors that we’ve come to associate with the term “ADHD.”

Thomas Armstrong

Cloverdale, Calif.

The writer is the author of The Myth of the ADD Child, and ADD/ADHD Alternatives in the Classroom.

To the Editor:

Your article on research developments related to ADHD was extremely interesting. Its contention that ADHD has a biological basis seems not contestable. However, numerous Diagnostic and Statistical Manual psychiatric disorders have a biological basis. All DSM-IV categories are fundamentally attempts at grouping attributes seen repeatedly in children and adults.

I could find nothing in the research referred to in the article that could clearly separate on the biological and neurochemical level ADHD from a number of other DSM-IV disorders. For example, imbalances in the neurotransmitter dopamine, which the article indicates “appear to be closely related to ADHD symptoms,” can also be seen in individuals with major depressive episodes, manic episodes, bipolar disorders, and more, according to the DSM-IV. Brain-scan analysis on the size of various parts of the brain may provide some level of discrete differences between numbers of conditions, but I could see no clear indication of this from the article.

As we who work in the field of special education know only too well, students with the medical diagnosis of ADHD are classified in a number of different ways by school districts. Some are identified as “learning disabled,” some as “other health impaired,” some as “seriously emotionally disturbed.” Many are not identified under the Individuals with Disabilities Education Act, but rather are provided accommodations under Section 504 of the Rehabilitation Act. Some get though school without ever having legal status as a student with a disability.

The article avoided some very serious issues for the education community. One that came to mind was this: On the etiological level, is there a significant difference between learning disabilities and ADHD for large numbers of students? How many students identified for educational purposes as seriously emotionally disturbed have the etiology for ADHD? Lastly, the article referred several times to the drug Ritalin produced by Novartis, but failed to explain the similarities between Ritalin, methylphenidate, and cocaine. Researchers, including Russell A. Barkley, who was referred to in the article, admit the similarity of Ritalin to these drugs in numerous places, yet the article failed to note this. Teachers and educators in general need to understand this aspect of Ritalin before they ever use the word.

In my work as part of a court- appointed monitoring team looking daily at the files of special education students in Chicago, I often see students who are being medically treated for ADHD. Sometimes they are labeled learning-disabled, other times something else. The diagnosis and medical treatment of ADHD does not for some of these students equate to improved performance. Educational systems, accommodations, modifications, and effective instruction may play a larger role in educational performance than does ADHD treatment, from what I have seen here in Chicago. Since Education Week is a paper for the education community, some research in that area should have been referred to in the article.

Rodney D. Estvan

Chicago, Ill.

The writer works as a consultant in the office of Judge Joseph Schneider, the court-appointed monitor in Corey H. v. The Chicago Board of Education, et. al.

A version of this article appeared in the May 30, 2001 edition of Education Week as Letters

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