Brain Changes in Patients With Focal Hand Dystonia

Objective The purpose of this study is to determine if in focal hand dystonia there is disinhibition involving key structures of the motor control system (basal ganglia, thalamus, cerebellum and motor cortex) caused by dysfunction of the GABA-ergic neurons. The major inhibitory neurotransmitter in the central nervous system is gamma-amino butyric acid (GABA), which acts mainly through GABA A receptors, the majority of which possess the benzodiazepine binding site. Pathological processes involving GABA-ergic neurons will cause alterations in the density of GABA receptors, which can be visualized and measured with positron emission tomography (PET) using as a radioactive ligand \[(11)C\] Flumazenil. Study Population This research will be conducted using 20 patients with primary focal hand dystonia and 20 healthy volunteers that are matched by age and gender. Design By using positron emission tomography (PET) using radioactive ligand \[(11)C\] Flumazenil, we will detect alterations in the density of GABA receptors in patients with primary focal hand dystonia in comparison with control subjects. Outcome Measures We will be able to determine the density of GABA A receptors of the various Regions of Interest as measured by PET analysis among these groups of subjects. This study should provide new information concerning localization and degree of dysfunction of GABA-ergic neurons in movement related structures in dystonia, which might open new possibilities for pharmacological treatment of this disorder.