The exact cause of ADHD is unknown, although abnormal neurotransmitter levels, genetics, and complications occurring around the time of birth have been implicated. According to the National Resource Center on ADHD, heredity makes the largest contribution to the prevalence of ADHD in the population. ADHD occurs frequently in families, and inheritance is an important risk factor. Between 10–35% of children diagnosed with ADHD have a first-degree relative with ADHD. Approximately 50% of parents who have ADHD have a child with the disorder. ADHD is significantly more likely to be present in an identical (monozyogotic) twin than in a fraternal (dizygotic) twin.
ADHD is not a form of gross brain damage. Because the symptoms of ADHD respond well to treatment with stimulants that increase the availability of the neuro-transmitter dopamine, the dopamine hypothesis has gained acceptance. The dopamine hypothesis suggests that ADHD is due to inadequate availability of dopamine in the central nervous system. Dopamine plays a key role in initiating focused movement, increasing motivation and alertness, and preventing sleepiness in response to boredom. Multiple genes have been implicated in ADHD, including genes affecting dopamine usage by the brain.
The male to female ratio is 8:1. Despite the strong genetic linkage, research also suggests that non-genetic factors may play a role in ADHD. Hyperactivity and inattention are more common in children who have had exposure to toxins such as lead, alcohol, or cigarette smoke, or episodes of fetal oxygen deprivation during complications of pregnancy. These factors may adversely affect dopamine-rich areas of the brain.
In addition to dopamine, research has shown that glucose usage may also be involved in ADHD. Brain-imaging studies, using a technique called magnetic resonance imaging (MRI), have demonstrated differences between the brains of children with and without ADHD. A link has been established between an individual's ability to pay continued attention and the brain's use of glucose as a fuel. In adults with ADHD, the brain areas that control attention span may use less glucose and be less active, suggesting that a lower level of activity in this part of the brain may cause the inattention symptoms associated with ADHD.
By 2002, the NIMH Child Psychiatry Branch had performed a decade-long controlled study that demonstrated ADHD children having 3–4% smaller brain volumes in multiple critical brain regions affecting the types of behaviors associated with ADHD. The study also demonstrated that ADHD children receiving medication had developed volume of white matter that was the same as normal children. Individuals who had ADHD but were never medicated had an abnormally small volume of white matter. Whether or not genetic differences are responsible remains to be determined. As of 2004, the NIMH is conducting clinical trials examining the MRI of identical twins with ADHD.
Maria Basile PhD, Thomson Gale, Gale, Detroit,