This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. A number of volumetric and functional brain imaging studies suggest abnormalities in neuronal circuits involving the cortex, striatum, and thalamus as a possible cause of Tourette syndrome. Although the measurement of N-acetylaspartate (NAA), a neuronal marker, through proton magnetic resonance spectroscopy (MRS) provides a unique opportunity for the in vivo investigation of neuronal abnormalities in these regions, there have been, to date, no published studies of NAA or proton MRS in Tourette syndrome. However, pilot data from our initial MRS study of Tourette syndrome suggests neuronal abnormalities in the caudate nucleus and frontal lobes and a lack of the normal asymmetry seen in the caudate nucleus and frontal gray matter. The objective of the present study is to confirm and extend these findings in Tourette syndrome using magnetic resonance imaging and magnetic resonance spectroscopy. Children and adolescents with Tourette syndrome and a control group of children without tics or other major psychiatric illness will undergo magnetic resonance scanning on a 3 Tesla head only magnetic resonance scanner. Frontal gray and white matter volumes and the volume of the basal ganglia and the thalamus will be measured on magnetic resonance images using semiautomated techniques. The concentration of NAA will be measured in these regions as well using magnetic resonance spectroscopy. We hypothesize that patients will have reductions in frontal gray matter volumes and caudate nucleus volumes. Patients will also have abnormalities of NAA in these regions and will lack the normal asymmetry of the caudate nucleus, suggesting neuronal abnormalities. If these hypotheses are confirmed, these findings would further our knowledge of the neurobiological basis of Tourette syndrome and may ultimately be important in determining more effective treatments for tics.
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