Biology 202
1999 First Web Reports
On Serendip

Attention Deficit Hyperactivity Disorder: Neurobiology of a Disorder or a Difference?

Lacey Tucker

Attention Deficit Hyperactivity Disorder (ADHD) is a phrase that has moved out of the realm of pure science or psychology and into common parlance. Like depression, the public has a general and vague sense of the "type" of person who may have ADHD, and has heard the name Ritalin, the main drug used in treatment, bandied about. As the name of the disorder implies, its symptoms present generally as "inattention and a combination of hyperactive and impulsive behaviors" (2). ADHD has only recently been able to be tangibly identified in the nervous system, and its' diagnostic criteria has continued to be revised. The discovery of specific physiological differences in the brain has enabled scientists to correlate the behavioral symptoms associated with ADHD with specific differences, mutations, or malfunctions in the brain. Though the scientific burden of proof cannot be ignored, the way in which we choose to define these differences as a "disorder" is debatable. Given both the scientific understanding of the sheer size of the nervous system and the more poetic notion of individuality, the neurobiological differences associated with ADHD are difficult to adequately define within the unlimited permutations of human personalities.

The current official American criteria for diagnosing the condition of ADHD, according to the DSM-IV, is based on a child presenting at least six symptoms of inattention, hyperactivity-impulsivity, or both, that have persisted for at least six months (3). Additionally, some symptoms must have been present before seven years of age, and some type of social, academic or occupational impairment must result from these symptoms in at least two different environments in which the child regularly interacts and performs tasks (3) . Specifically, the following functions are thought to be impaired: nonverbal working memory, internalization of self-directed speech, self-regulation of mood, motivation and level of arousal, and reconstitution (the ability to break down observed behaviors...that can be recombined...in pursuit of a goal" (11). Despite the newfound specificity of the symptoms, many still believe that ADHD is difficult to accurately diagnose. These "symptoms" can also be the sign of a person whose personality is creative, quick and high-energy. One of the many controversies surrounding ADHD is the inaccurate labeling of a child who may not have a disorder but merely a distinctive personality. Put more concisely, where do we draw the line between "personality and pathology?" (9)

Recent research aiming to define the physiological parameters of ADHD has succeeded in indicating ways in which aspects of brain activity, size and functioning differ from people without symptoms of the disorder. ADHD is now seen primarily as "A developmental failure of the brain circuitry that underlies inhibition and self-control" (2). The areas thought to be affected are the prefrontal cortex and at least two deeply embedded clusters of nerve cells called the basal ganglia. A 1996 study at the National Institute of Mental Health found that the two basal ganglia called the globus pallidus and the caudate nucleus, as well as the anterior frontal part of the brain, are smaller in size in ADHD children (3)(10). These are the regions of the brain involved in regulating attention, ignoring distractions and "editing behavior" (2). Positron emission tomography (PET) has shown that ADHD brains consume less energy in certain regions, including the frontal lobes of the cerebral cortex (1). If the brain equals behavior, (e.g., different vertebrates with physically different brains exhibit different behaviors), a tangible physical difference in the brains of humans who exhibit ADHD behavior supports this concept.

It has also become clear that there is an underlying genetic mutation and that it is heritable, so that families will present similarities in their ADHD behavior. This genetic mutation appears to cause differences in the synthesis of both dopamine transporters and receptors, which affects the way in which certain parts of the brain can communicate with each other, which affects their functioning. A mutation in the gene that synthesizes dopamine transporters can make them so effective that they perform reuptake of the neurotransmitter out of the synapse before it can adequately bind to receptors. A mutation of the gene that synthesizes the dopamine receptor makes it difficult for the dopamine to bind at all. In either case, the neurotransmitter will be less effective and the propagation of the action potential in the post-synaptic neuron will be less successful. Tellingly, the neurotransmitter dopamine has been found to be secreted specifically in parts of the brain whose functions are related to "inhibiting or modulating the activity of other neurons, particularly those involved in emotion and movement" (2). This experimental finding links the internal biology with the resulting external behaviors as described by the diagnostic criteria of the disorder. (See (6) for an excellent image of the above structures).

The most common and effective drug treatment is methylphenidate (Ritalin), which is a mild stimulant to the central nervous system. The specific way in which the drug stimulates the human nervous system isn't completely understood (7). One likely explanation, especially given the mounting scientific evidence of the malfunctions identified with ADHD, is that the neurotransmitter's rate of release or reuptake is adjusted, or that the brain's sensitivity (i.e. the receptor) is adjusted (9). According to one source, 70% of ADHD kids respond to this type of stimulant drug therapy (9).

The possible over-prescription of Ritalin continues to be a controversial subject, judging by the recent articles appearing in Time and The New Yorker (within the last two months). However, one reason that ADHD is regarded as a neurobiological disorder is actually because of the obvious positive effect that medications like Ritalin have on the symptoms. The usefulness of drug treatment is touted by some: "Teachers and therapists need to continue to do everything they can to help individuals with ADHD, but we need to realize that if we don't alter the biological factors that affect ADHD, we won't see much change (8)." On the other hand, there are people who believe that ADHD is a catchall for any child whose behavior is considered disruptive, and that medicating so many children for a disorder that it so difficult to accurately diagnose is dangerous and unethical. This is particularly poignant since it has been shown that ADHD symptoms aren't necessary for Ritalin to have an effect (9), leaving the door open for misuse.

It is clear that the availability of Ritalin has enabled individuals who honestly suffer from the symptoms of ADHD to achieve successes in school, career, and personal life that might be otherwise impossible due to their decreased ability to focus and organize. On the other hand, given the range of behaviors and personalities that the anatomy of the human nervous system makes possible, at what point are these behaviors deemed disorders? It is inevitable that we must question the use of a labeled "disorder" and the negative connotations that accompany this type of labeling. Some have called it "a misuse of psychiatric terminology to suppress natural liveliness" or "an administrative label applied to children...who are doing badly in school" (1). One could argue that the ADHD symptoms are interpreted negatively only within the boundaries of the environment in which we live. For instance, there is a documented difference in the number of children labeled ADHD in North America compared with the number in European countries. The British Psychological Society recently published a report warning practitioners in England not to follow the example of the United Stated and Canada in diagnosing children as ADHD based on so many diverse behaviors. The report comments that the diagnosis has become so often used that "it has a prominent place in the contemporary culture" (5). As the cultural climate of the United States stresses high achievement and a strong work ethic, and as its citizens are the product of an educational system that stresses conformance to the norm, then the personality type associated with ADHD will be interpreted as a neurological disorder, instead of a neurological difference. In fact, there is a website (borntoexplore.org) entirely devoted to looking at ADHD from this perspective. Posted there is a paper by Bonnie Cramond, Ph.D., who explores the close relationship between the personality type of the creative individual and the symptoms associated with ADHD (4). She cites several famous creative individuals such as Virginia Woolf, Frank Lloyd Wright and Thomas Edison who had inattentive or hyperactive personalities, but who were viewed as creative because of the uniqueness of their contributions. She draws connections to traits found in both creative and ADHD personalities, such as sensation seeking, sensitivity to stimulation, and depression. She cautions parents and teachers "to look carefully at behaviors exhibited by children for what may be potentialities instead of deficiencies" (4).

The social implications for educational and social success for the ADHD child are perhaps the most important point. After all, it is the individual child, regardless of the exact definition and nature of the disorder, who must live with the deficiencies and with the label. The majority of advice is to place children with ADHD in environments that promote the structure and routine that they lack internally (9) (1).(2). This is typically advised as a complement to drug treatment, which succeeds in temporarily altering the child's neural pathways to stimulate a greater sense of rules and inhibitory behavior. Some research, however, asserts that a high-energy personality should have "arousing, unstructured creative teaching to perform best" (4). This advice points to the inability for certain types of environmental input to achieve the desired long-term output due to differences in biology. The identification of a genetic component responsible for the physiological differences identified with ADHD raises the idea of the central pattern generator that individuals are born with. The crux of the matter is whether a child should be placed in a learning environment that is at odds with her internal construct. Regardless of any environmental input attempting to organize or calm ADHD behavior, the neural pathways will not change, or "learn" the desired behavior in its place. This, however, is arguable, as some people assert the ADHD behavior lessens with age. Others assert that it manifests differently, but that it is does exist in adults and is seen in symptoms such as impatience, restlessness, moodiness, insecurity and boredom (1). What seems abundantly clear, however, for the ADHD child, is that "praise is vitally important" (9). This is the type of difference that environmental input can make, so that children don't feel like failures.

WWW Sources

1) article from "The Harvard Mental Health Letter"

2)"Scientific American" article by Russell A. Barkley

3) DSM-IV diagnostic criteria

4) fabulous paper by Bonnie Craymond linking ADHD and the creative personality

5) article from "The Medical Post" by Harvey McConnell

6) great graphic

7) pharmacology information on Ritalin

8) list of myths and corrections about ADHD

9) article from "Time" by Claudia Wallis

10)"Scientific American" article by Kristin Leutwyler

11) part of Barkley article diagramming a psychological model of ADHD




| Course Home Page | Back to Brain and Behavior | Back to Serendip |

Send us your comments at Serendip
© by Serendip 1994- - Last Modified: Monday, 07-Jan-2002 14:39:31 EST

This paper reflects the research and thoughts of a student at the time the paper was written for a course at Bryn Mawr College. Like other materials on Serendip, it is not intended to be "authoritative" but rather to help others further develop their own explorations. Web links were active as of the time the paper was posted but are not updated.

Contribute Thoughts | Search Serendip for Other Papers | Serendip Home Page