Prognostic Value of FP-CIT-SPECT in Parkinson´s Disease

Parkinson´s Disease

Parkinson´s disease, FP-CIT-SPECT

The investigators aim to study whether the nuclear medicine method FP-CIT-SPECT (more details see below) allows to predict the further clinical course of Parkinson´s disease. Especially the investigators are interested in the motor and cognitive functions of the parkinsonian patients.

Background of this study: Parkinson´s disease (PD) is a degenerative disorder of the nervous system. In PD, mainly the presynaptic dopaminergic neurons are affected: The dopamine synthesis as well as the active transport of dopamine into the synaptic gap by presynaptic dopamine transporters (DAT) is reduced. First parkinsonian symptoms occur when the concentration of dopamine within the basal ganglia is reduced by at least 80 per cent (Bernheimer et al. 1973). The reduced DAT density represents a typical phenomenon of PD. The DAT density can be measured by means of nuclear medicine methods: the tracer FP-CIT (Fluoropropyl-Carbomethoxy-Iodophenyl-Tropane) has a high affinity to presynaptic DAT (Booij et al. 1998). PD patients show a significantly lower striatal FP-CIT uptake than healthy controls. Therefore FP-CIT SPECT supports the diagnosis of PD (Benamer et al. 2000). Aims of this study: To test the predictive value of FP-CIT-SPECT concerning the clinical course of PD. Study protocol: In this study we now (time 2) examine 25 PD patients who where diagnosed as having PD and who underwent FP-CIT-SPECT in the years 2003 up to 2006 (time 1). At both times - time 1 and time 2 - the part III (motor part) of the Unified Parkinson´s Disease Rating Score (UPDRS-Score) was / will be performed in the Off state. Furthermore, at time 2 the CERAD examination will be performed. 25 patients have to be included, if a correlation coefficient r = 0.5, an error 1st order = 0.05 and an error 2nd order = 0.20 are assumed. We intend to answer the following questions: 1. Is there a correlation between the DAT density - measured between 2003 and 2006 - and the then (time 1) clinical symptoms hypokinesia, rigidity, resting tremor, postural tremor (measured by the motor part of the UPDRS scale)? 2. Is there a correlation between the DAT density - measured between 2003 and 2006 - and the actual (year 2010, time 2) clinical symptoms hypokinesia, rigidity, resting tremor, postural tremor? 3. Is there a correlation between the DAT density - measured between 2003 and 2006 - and the change of clinical symptoms hypokinesia, rigidity, resting tremor, postural tremor 2003-2006 versus 2010 (delta = time 2 - time 1). 4. Is there a correlation between the DAT density - measured between 2003 and 2006 - and the actual (year 2010, time 2) cognitive functions (measured by the CERAD)?

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