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NEUROLOGY 2005;64:347-349
© 2005 American Academy of Neurology


Brief Communications

Decreased striatal D2 receptor binding in non-manifesting carriers of the DYT1 dystonia mutation

K. Asanuma, MD, Y. Ma, PhD, J. Okulski, BS, V. Dhawan, PhD, T. Chaly, PhD, M. Carbon, MD, S. B. Bressman, MD and D. Eidelberg, MD

From the Center for Neurosciences (Drs. Asanuma, Ma, Dhawan, Chaly, Carbon, and Eidelberg, and J. Okulski), North Shore–Long Island Jewish Research Institute; Department of Neurology (Drs. Ma, Dhawan, Chaly, and Eidelberg), North Shore University Hospital and New York University School of Medicine; and Department of Neurology (Dr. Bressman), Beth Israel Medical Center, New York, NY.

Address correspondence and reprint requests to Dr. David Eidelberg, Center for Neurosciences, North Shore–Long Island Jewish Research Institute, 350 Community Drive, Manhasset, NY 11030; e-mail: david1{at}nshs.edu

To determine whether reduced striatal D2 receptor binding reported in patients with idiopathic torsion dystonia is associated with the genotype, the authors used PET and [11C]-raclopride to assess non-manifesting carriers of the DYT1 mutation. D2 receptor binding was reduced by approximately 15% in caudate and putamen (p < 0.005). These results suggest that striatal D2 binding reductions are a trait feature of the DYT1 genotype.


Supported by NIH RO1 NS 37564 and the Bachmann-Strauss Dystonia and Parkinson Foundation.

Received April 9, 2004. Accepted in final form August 30, 2004.




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