Address for correspondence: Pedro Rosa Neto, M.D., PET Center, Århus Kommunehospital, Nørrebrogade 44, Århus, Denmark.
pedro{at}pet.auh.dk
Ann. N.Y. Acad. Sci. 965: 434-439 (2002).
Perinatal anoxia/ischemia or premature birth increases the risk
of developing attention deficit/hyperactivity disorder (ADHD).
Brain imaging studies of idopathic ADHD reveal elevated dopamine
transporter density in striatum of patients, predicting abnormal
response to a challenge with methylphenidate in this population.
We hypothesized that the severity of attention deficit in adolescents
should correlate with the sensitivity to psychostimulant-evoked
dopamine release. To test this hypothesis, we investigated six
adolescent subjects (mean age 14.2 ± 2.4 yr) with documented
birth trauma and/or low birth weight and a diagnosis of ADHD.
Using positron emission tomography (PET), we measured the relative
binding of [
11C]raclopride to dopamine receptors in striatum,
first in the baseline condition and again after methylphenidate
challenge at a therapeutic dose for ADHD (0.3 mg/kg, p.o.) in
order to map the altered dopamine release evoked by the psychostimulant
challenge. Neuropsychological measurements of impulsivity and
inattention were also performed. We found a positive correlation
between commission errors and the methylphenidate-evoked decrease
in [
11C]raclopride binding, thought to reflect the balance of
dopamine release and reuptake. The greater the decline in the
[
11C]raclopride binding, the greater the ability of methylphenidate
to block the reuptake of dopamine. As the ability to block the
reuptake depends on the relative dopamine concentration, the
result suggests that the impulsivity in these adolescents is
associated with abnormally low extracellular dopamine concentration.
