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Neurology 2003;61:310-315
© 2003 American Academy of Neurology

Increased ventral striatal monoaminergic innervation in Tourette syndrome

R.L. Albin, MD, R.A. Koeppe, PhD, N.I. Bohnen, MD PhD, T.E. Nichols, PhD, P. Meyer, MD, K. Wernette, MSN, S. Minoshima, MD PhD, M.R. Kilbourn, PhD and K.A. Frey, MD PhD

From the Departments of Neurology (Drs. Albin and Frey, and K. Wernette) and Radiology (Nuclear Medicine) (Drs. Koeppe, Bohnen, Meyer, Minoshima, Kilbourn, and Frey, and K. Wernette), The University of Michigan Medical School, Ann Arbor; Geriatric Research, Education and Clinical Center (Dr. Albin), Veterans Administration Medical Center, Ann Arbor; Department of Biostatistics (Dr. Nichols), The University of Michigan School of Public Health, Ann Arbor; and Department of Radiology (Dr. Minoshima), University of Washington, Seattle.

Address correspondence and reprint requests to Dr. Roger L. Albin, 4412D Kresge III, 200 Zina Pitcher Place, Ann Arbor, MI 48109-0585; e-mail: ralbin{at}umich.edu

Background: Excessive striatal dopaminergic innervation is suggested to underlie Tourette syndrome (TS). Prior imaging and postmortem studies yield conflicting data.

Methods: The authors used PET with the type 2 vesicular monoamine transporter ligand [11C]dihydrotetrabenazine (DTBZ) to quantify striatal monoaminergic innervation in patients with TS (n = 19) and control subjects (n = 27). Compartmental modeling was used to determine blood to brain ligand transport (K1) and tissue to plasma distribution volume (a measure of ligand binding) during continuous infusion of DTBZ. TS data were compared with control data using predefined regions of interest and on a voxel by voxel basis.

Results: There were no significant differences in ligand binding or ligand transport between patients with TS and control subjects in the dorsal striatum. With voxel by voxel analysis, there was increased DTBZ binding in the right ventral striatum.

Conclusions: Previously reported differences between patients with TS and control subjects in dorsal striatal dopamine terminal markers may reflect medication-induced regulation of terminal marker expression or be the result of intrinsic differences in striatal dopaminergic synaptic function. Increased right ventral striatal DTBZ binding suggests that abnormal ventral striatal dopaminergic innervation may underlie tics.




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