For the first time, scientists have a neurobiological explanation for the variation in severity of tics in Tourette Syndrome. Researchers at the National Institute of Mental Health have traced such symptom differences to "supersensitivity" of certain neurotransmitter receptors in the brain structure responsible for carrying out automatic behaviors. They suggest that this dysfunction may underlie the compulsion to act out the sudden movements and vocalizations that characterize Tourette Syndrome, which affects about 100,000 Americans with its full-blown form and up to 0.5% of the population with milder symptoms. The researchers report on their findings in the August 30th issue of Science.
In a brain imaging study of identical twins differently affected by the disorder, Daniel Weinberger, M.D., Steven Wolf, M.D., and colleagues in the NIMH Clinical Brain Disorders Branch found that binding to D2 dopamine receptors in the caudate nucleus was higher in the sibling with the more severe symptoms.
"Strikingly, the degree to which the twins differed in this caudate D-2 binding predicted almost absolutely their differences in tic severity," said Weinberger. "This also likely explains the ebb and flow of tics experienced over the course of Tourette Syndrome and its overlap with obsessive compulsive disorder.
"While we know that genetics plays an important role in transmission of Tourette Syndrome, the fact that identical twins show differences in symptom severity suggests that environmental influences modify the clinical expression of the disorder," he explained. "We studied identical twins discordant for such symptom severity to control for normal genetic variation in brain function."
Although previous studies comparing unrelated Tourette patients with unaffected
persons had failed to show differences in dopamine system function, the NIMH
Contact: Jules Asher
NIH/National Institute of Mental Health