It has long been thought there must be a measurable
anatomical difference in the brains of those with attention deficit disorder (ADHD).
As imaging technology has advanced over the years, many studies have put this theory to the test with increasingly sophisticated results.
One of the latest studies examining structural differences in the brains of individuals with ADHD uses Magnetic Resonance Imaging (MRI). This study scanned 104 people with ADHD and 47 without and found some significant differences between the two groups.
Among those with ADHD, an area of the brain called the putamen (in the basal ganglia) showed significantly smaller volume than in the control group—suggesting anatomical dysregulation in the circuitry of the basal ganglia and also suggesting that stimulant medication normalized those features in those with the disorder.
These and other findings have led to a theory about the cause of ADHD. Some now believe an abnormal gene (perhaps the dopamine-transporter gene) may lead to low levels of dopamine at the synapses in the basal ganglia of the brain. This gene provides the blueprint for proteins involved in removing dopamine from the synaptic cleft through a re-uptake mechanism—these proteins are known to occur at abnormally high levels in people with ADHD.
With more than a normal amount of dopamine being removed, deficits of this chemical occur. Deficits in dopamine produce anatomical alterations including a reduction in the number of synapses, a decreased number of dendrite spines on brain cells and decreases in the branching length of dendrites. These cellular changes could produce local volume reduction in the basal ganglia that we can now detect with MRI.
The putamen is the largest recipient of dopamine neurons in this area of the brain and this structure supports the acquisition and execution of a broad range of behavioural actions that are abnormal in those with ADHD. Some of these include context inappropriate behaviour, deficits in working memory and impaired motor control.
Stimulant medications used widely in the treatment of ADHD increase the level of dopamine in these critical areas by blocking the re-uptake of dopamine. This then leads to a reversal of some of the anatomical changes discussed above and brings about the associated improvement in behaviour.
Now that researchers have identified these physical differences, we can use this information to develop even better treatments. For example, a medication that is more selective to this dopamine re-uptake mechanism and area of the brain would have a better balance of benefits to side effects.
A medication that turns down the volume of dopamine transporter units in this area of the brain would be even better. The more we learn, the more research can be done. It is just a matter of time until we can develop a highly targeted and effective treatment for this condition that affects so many.
Still, existing treatments can improve functioning as well as reverse some of the brain changes that take place as part of this disorder.
Paul Latimer is a psychiatrist and president of Okanagan Clinical Trials.