HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Asanuma, K. Articles by Eidelberg, D. Search for Related Content PubMed PubMed Citation Articles by Asanuma, K. Articles by Eidelberg, D. Related Collections PET Dystonia All Genetics

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

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.

This article has been cited by other articles:

				U. Muller The monogenic primary dystonias Brain, August 1, 2009; 132(8): 2005 - 2025. [Abstract] [Full Text] [PDF]

				M. Carbon, M. Niethammer, S. Peng, D. Raymond, V. Dhawan, T. Chaly, Y. Ma, S. Bressman, and D. Eidelberg Abnormal striatal and thalamic dopamine neurotransmission: Genotype-related features of dystonia Neurology, June 16, 2009; 72(24): 2097 - 2103. [Abstract] [Full Text] [PDF]

				A Quartarone, F Morgante, A Sant'Angelo, V Rizzo, S Bagnato, C Terranova, H R Siebner, A Berardelli, and P Girlanda Abnormal plasticity of sensorimotor circuits extends beyond the affected body part in focal dystonia J. Neurol. Neurosurg. Psychiatry, September 1, 2008; 79(9): 985 - 990. [Abstract] [Full Text] [PDF]

				M. Carbon, M. F. Ghilardi, M. Argyelan, V. Dhawan, S. B. Bressman, and D. Eidelberg Increased cerebellar activation during sequence learning in DYT1 carriers: an equiperformance study Brain, January 1, 2008; 131(1): 146 - 154. [Abstract] [Full Text] [PDF]

				A. Feigin, C. Tang, Y. Ma, P. Mattis, D. Zgaljardic, M. Guttman, J. S. Paulsen, V. Dhawan, and D. Eidelberg Thalamic metabolism and symptom onset in preclinical Huntington's disease Brain, November 1, 2007; 130(11): 2858 - 2867. [Abstract] [Full Text] [PDF]

				J. S. Perlmutter and W. T. Thach Writer's cramp: Questions of causation Neurology, July 24, 2007; 69(4): 331 - 332. [Full Text] [PDF]