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CHAPTER 12 - IMAGES OF ATTENTION DEFICIT DISORDER
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The first evidence for the brain being under stimulated was introduced with the use
of more advanced electroencephalograms (EEG or brainwave studies) by Joel Lubar from
the University of Tennessee. He demonstrated that when ADD children and teenagers
performed a concentration task there was an increased amount of slow brain wave
activity in their frontal lobes, instead of the usual increase in fast brain wave
activity that was seen in the majority of the control group.
In 1990, published PET data that supported the notion of brain underactivity in the
prefrontal cortex, especially in response to an intellectual challenge. Data from my
own work with SPECT brain imaging drew the same conclusions. At rest most ADD people
have normal activity in their brain. When they perform a concentration task,
however, they experience decreased activity in the prefrontal cortex, rather than
the expected increased activity that is seen in a normal control group.
Tied to the decreased prefrontal cortex findings are the studies that indicate that
ADD is has a large genetic contribution, involving dopamine availability in the
brain. A significant amount of dopamine is produced in the basal ganglia (large,
structures deep within the brain). Stimulant medications work by enhancing dopamine
availability in this part of the brain. Studies have demonstrated that the basal
ganglia is smaller in people with ADD. 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.
Beside the genetic contribution to ADD, 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.
Subtypes of ADD
It is essential to note that ADD is a developmental disorder diagnosed through
clinical history over a prolonged period of time. Brain imaging is not necessary to
make the diagnosis of ADD, although it may be helpful in certain complicated cases.
Based on my brain imaging experience I have seen 7 clinical subtypes of ADD:
1. AD/HD, combined type with both symptoms of inattention and
hyperactivity-impulsivity. SPECT Brain imaging typically shows decreased activity in
the basal ganglia and prefrontal cortex during a concentration task. This subtype of
ADD typically responds best to psychostimulant medication.
2. AD/HD, primarily inattentive ADD subtype with symptoms of inattention and also
chronic boredom, decreased motivation, internal preoccupation and low energy. Brain
SPECT imaging typically shows decreased activity in the basal ganglia and dorsal
lateral prefrontal cortex during a concentration task. This subtype of Inattentive ADD also
typically responds best to psychostimulant medication.
3. Overfocused ADD, with symptoms of trouble shifting attention, cognitive
inflexibility, difficulty with transitions, excessive worrying, and oppositional and
argumentative behavior. There are often also symptoms of inattention and
hyperactivity-impulsivity. Brain SPECT imaging typically shows increased activity in
the anterior cingulate gyrus and decreased prefrontal cortex activity. This subtype
of Overfocused ADD typically responds best to medications that enhance both serotonin and dopamine
availability in the brain, such as venlafaxine or a combination of an SSRI (such as
fluoxetine or sertraline) and a psychostimulant.
4. Temporal lobe ADD, with symptoms of inattention and/or
hyperactivity-impulsivity and mood instability, aggression, mild paranoia, anxiety
with little provocation, atypical headaches or abdominal pain, visual or auditory
illusions, and learning problems (especially reading and auditory processing). Brain
SPECT imaging typically shows decreased or increased activity in the temporal lobes
with decreased prefrontal cortex activity. Aggression tends to be more common with
left temporal lobe abnormalities. This subtype of Temporal ADD typically responds best to
anticonvulsant medications (such as gabapentin, divalproate, or carbamazepine and a
psychostimulant.
5. Limbic ADD, with symptoms of inattention and/or hyperactivity-impulsivity
and negativity, depression, sleep problems, low energy, low self-esteem, social
isolation, decreased motivation and irritability. Brain SPECT imaging typically
shows increased central limbic system activity and decreased prefrontal cortex
activity. This Limbic ADD subtype typically responds best to stimulating antidepressants such
as buprion or imipramine, or venlafaxine if obsessive symptoms are present.
6. Ring of Fire ADD - many of the children and teenagers who present with
symptoms of ADD have the "ring of fire" pattern on SPECT. They often do
not respond to psychostimulant medication and in many cases are made worse by them.
They tend to improve with either anticonvulsant medications, like Depakote or
Neurontin, or the new, novel antipsychotic medications such as Risperdal or Zyprexa.
The symptoms of this pattern tend to be severe oppositional behavior,
distractibility, irritability and temper problems and mood swings. We think it may
represent an early bipolar pattern.
top down active view
increased activity in the cingulate,
lateral parietal, frontal and temporal lobes |
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active front on view
increased activity in the cingulate,
lateral parietal, frontal and temporal lobes |
top down active view
increased activity in the cingulate,
lateral parietal, frontal and temporal lobes |
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left side active view
increased activity in the cingulate,
lateral parietal, frontal and temporal lobes |
7. Trauma Induced ADD, especially to the left dorsolateral prefrontal cortex.
The symptoms come on or intensify in the year after a head injury or brain trauma. The ADD symptoms
may respond to psychostimulant medication. If irritability results secondary to
psychostimulant medication the addition of a low dose anticonvulsant may be
helpful.
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