"Recent imaging and postmortem studies now implicate the ventral striatum and caudate nucleus--two regions of the basal ganglia--as areas associated with the brain dysfunction seen in Tourette's," says Neal Swerdlow, MD, PhD, of the University of California-San Diego department of psychiatry, co-chair of a symposium at this meeting titled "Tourette's: The Self Under Seige."
"Although there is general agreement that the basal ganglia are implicated in Tourette's syndrome, we know relatively few details. For example, we know that increased activation in the caudate and prefrontal cortex is associated with better tic control," says James Leckman, MD, of the Yale University School of Medicine Child Study Center and co-chair of the symposium. "There is also evidence that the actual size of the caudate nucleus is reduced in many individuals with Tourette's. But we don't know how these findings are linked to the clinical features of Tourette's including its waxing and waning course and why the tic symptoms usually peak in early adolescence."
Knowing that dopamine antagonist drugs reduce the tics associated with Tourette's and that selective serotonin reuptake inhibitors reduce the symptoms of obsession and compulsions, Roger Albin, MD, and colleagues at the University of Michigan department of neurology investigated the idea that the ventral striatum--a brain region where both dopamine and serotonin have important functions--could be involved in Tourette's syndrome.
Noninvasive imaging studies show that the ventral striatum of Tourette's patients has an excessive amount of dopamine-containing nerve terminals. Other studies suggest that in normal brain development, dopamine-containing nerve terminals are overproduced in the years leading up to adolescence, and that these nerve terminals are pruned back during adolescence.