Program Twentieth Annual Symposia on Etiology, Pathogenesis, and Treatment of Parkinson’s Disease and Other Movement Disorders Cosponsored by the Parkinson Study Group, Huntington Study Group, Dystonia Study Group, Myoclonus Study Group, Tourette Syndrome Study Group, Cooperative Ataxia Group, Tremor Research Group, and The Movement Disorder Society This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through joint sponsorship of The Movement Disorder Society and the Parkinson Study Group. The Movement Disorder Society is accredited by the ACCME to provide continuing medical education for physicians. The symposia will consist of peer-reviewed platform and poster presentations designed to communicate recent research advances in the field of Parkinson’s disease, Huntington’s disease, ataxia, dystonia, myoclonus, Tourette’s syndrome, tremor and other Movement Disorders to professionals in neurology and related disciplines. Practitioners, educators, and researchers are invited to attend. Abstracts of platform and poster presentations representing original material will be published in the September 2006 issue of Movement Disorders. At the conclusion of this session, participants should be able to: 1) Identify by scholarly review, oral presentation and group discussion the current research into the diagnosis, prevention and treatment of Parkinson’s disease and other Movement Disorders; 2) Identify the important advances in research and clinical treatments relating to a variety of Movement Disorders; 3) Discuss new pharmacological and non-pharmacological treatment options available for Parkinson’s disease and other Movement Disorders; 4) Identify the mechanisms (genetic, environmental, pathophysiology, neurobiology) linked to Parkinson’s disease and other Movement Disorders; and 5) Discuss the diagnostic approaches and tools available for Parkinson’s disease and other Movement Disorders. MORNING SESSION: 8:15 AM-NOON The morning session consists of a keynote speaker and 11 presentations by the following individuals with allotted time for questions and answers after each presenter. 8:15-9:00 AM KEYNOTE ADDRESS: New Insights Into the Etiology of Parkinson’s Disease and Symptom-Linked Adaptations D. James Surmeier, PhD. Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. 9:00-9:15 AM Gene Therapy for Parkinson’s Disease with Subthalamic Nucleus AAV-GAD: FDG PET Results A. Feigin, 1 C. Tang, 1 M. During, 2 M. Kaplitt, 2 D. Eidelberg. 1 1 Feinstein Institute for Medical Research, North Shore– LIJ Health System, Manhasset, NY; 2 Weill–Cornell Medical Center, New York, NY, USA. Objective: To assess changes in brain metabolism in a clin- ical trial of unilateral adeno-associated virus vector delivery of the glutamic acid decarboxylase gene (AAV-GAD) into the subthalamic nucleus (STN) in Parkinson’s disease (PD). Back- ground: As part of an open-label trial of unilateral STN AAV- GAD in 12 PD patients (age 58.2  5.7), we performed FDG PET at baseline and after 6 and 12 months. Design/Methods: FDG PET scans were analyzed using SPM: 1) To compare regional metabolism at 6 and 12 months versus baseline and 2) To correlate changes in UPDRS ratings at each time point with regional metabolism. We also used network analysis to assess the effects of therapy on the expression of the PD-related covariance pattern (PDRP) on a hemisphere basis. Results: Baseline, 6- and 12-month “off” motor UPDRS scores were 38.6  8.4, 28.7  12.3 (P = 0.01) and 29.7  13.6 (P = 0.02). Five subjects appeared to respond (UPDRS improve- ment  40%, mean 52%  10%), but 7 did not (improvement 25%, 2%  21%). Brain metabolism declined in internal globus pallidus and ventrolateral thalamus ipsilateral to AAV- GAD. UPDRS improvements correlated with increased metab- olism in premotor and supplementary motor regions (R=-0.84 P  0.001) ipsilateral to AAV-GAD. Changes in PDRP expression correlated with improvement in UPDRS mo- tor ratings (R = 0.45, P = 0.03; Bland-Altman within-subject correlation), with greater suppression in the clinical responders (P  0.01). Conclusion: These imaging results suggest that Published online in Wiley InterScience (www.interscience.wiley. com). DOI: 10.1002/mds.21133 Movement Disorders Vol. 21, No. 10, 2006, pp. 000 – 000 © 2006 Movement Disorder Society