EP 76. Striatal dopamine transporter availability and clinical course in Parkinson’s disease patients with deep brain stimulation of the subthalamic nucleus within one-year follow-up

Abstract

Introduction Degeneration of dopaminergic neurons in the substantia nigra projecting to the striatum is responsible for the motor symptoms in Parkinson's disease (PD). Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a well-established procedure to alleviate these symptoms in advanced PD. Yet the mechanism of action, especially the effects of DBS on striatal dopamine transporter (DAT) availability, remains largely unknown. Objectives The aim of our study was therefore to evaluate whether (1) DAT availability changes within one year after DBS and whether (2) the clinical outcome is predictable by DAT availability before surgical procedure (pre-op). Patients and methods Twenty-nine PD patients (age: 62.3±8.7y; duration of illness: 12.9±4.8y; L-dopa equivalent dose LED: pre 943±465mg, post 313±206mg; motor score UPDRS III pre ON (LED): 25.8±12.0, pre OFF: 42.0±14.6, post ON (LED+DBS): 15.9±9.1, post OFF: 40.1±14.0) underwent [ 123 I] FP-CIT SPECT prior and one year after STN-DBS. DAT availability (specific-to-unspecific binding ratio SBR) was assessed by volume of interest- (VOI; PMOD 3.4; caudate nucleus; putamen) and a voxel-based analysis. SBR were correlated with the severity of disease (UPDRS III). Results (1) UPDRS III improved significantly one year after STN-DBS (ON-state p =0.006) while in parallel LED was reduced ( p p r =−0.01; p =0.972; ON putamen ON: r =−0.31; p =0.898). Conclusion In accordance with own previous findings (Hesse et al., 2008), DAT availability is stable one-year after STN-DBS. However, DAT availability pre-op did not predict the clinical outcome after this follow-up period under STN-DBS. Whether a subtype-specific pattern of pre-op DAT availability helps to distinguish between responder and non-responder has to be evaluated in larger study cohorts. At this time the meaning of DAT alteration in the ventral striatum is unclear; a correlation to neuropsychiatric symptoms is assumed but this hypothesis needs further exploration as well.