ADD / ADHD Subtypes

Using advanced EEG in the 1980s, Joel Lubar, PhD introduced the first evidence demonstrating that the brains of children and teenagers with ADD had decreased activity during a concentration task. He found that there were more slow brain waves in their frontal lobes, instead of the usual fast brain wave activity with concentration that was seen in most of the control group.In 1990, Alan Zametkin, MD published data from positron emission tomography (PET) studies that supported the notion of brain underactivity in the prefrontal cortex, especially in response to an intellectual challenge. Data from our own work with brain SPECT imaging drew the same conclusions.

At rest, most ADD scans show normal activity in the brain but when performing a concentration task, there is decreased of activity in the prefrontal cortex, rather than the expected increase that is seen in a normal control group.

Research indicates that ADD has a large genetic influence involving dopamine availability in the brain. A significant amount of dopamine is produced in the basal ganglia. The basal ganglia have a significant number of nerve tracks that go through the limbic system to the prefrontal cortex. It appears that when there is not enough dopamine available in the basal ganglia then there is not enough “fuel” to drive the frontal lobes when they need to activate with concentration.

In addition to genetics, maternal alcohol or drug use, birth trauma, jaundice, brain infections and head trauma (sometimes even minor ones, especially to the left prefrontal cortex) can play a causative role in ADD. Furthermore, there are numerous other factors in our society now that contribute to the rise of ADD in the population. These include an increase in processed foods and lower fat in the diet, excessive television and computer (including phone and tablet) time, video games and decreased exercise.

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