Lack of association between striatal dopamine receptor availability and cerebral glucose metabolism in PSP

Objectives Accurate diagnosis of progressive supranuclear palsy (PSP) is of high clinical relevance. Currently, both IBZM SPECT and FDG PET are used for this purpose, which frequently show a reduced striatal dopamine D2 receptor (D2R) binding and a distinctive pattern of mesio- and dorsofrontal hypometabolism, respectively. This study investigates if IBZM SPECT and FDG PET depict independent disease features in PSP.

Methods IBZM SPECT and FDG PET scans of 8 patients with clinical and imaging findings highly suggestive of PSP were analyzed: For evaluation of D2R binding, the side-average distribution volume ratio (DVR) of striatum to frontal cortex (reference region) IBZM uptake was calculated (DVR-mean). Furthermore, maximum DVR (bilateral circular ROI of 5 mm diameter; DVR-max) was determined to minimize partial volume effects. DVR data were correlated voxel-wise with cerebral FDG uptake using Statistical Parametric Mapping (SPM2; proportional scaling, 10 mm Gaussian filter).

Results At an explorative statistical threshold of p-voxel<0.05 and clustersize>100 voxel several clusters with positive correlation between DVR-mean and FDG uptake were found in a rim-like shape along the surface of right frontal and left cerebellar cortex, corpus callosum, lateral ventricles, as well as brainstem and third ventricle. There were no correlation clusters clearly localized within gray matter. No negative correlation between DVR-mean and FDG uptake was detected. There was no correlation between DVR-max and FDG uptake.

Conclusions The shape and localisation of the detected correlation clusters strongly suggest that they are caused by atrophy. In line with this, MRI volumetry studies show a considerable brain volume loss in the aforementioned areas and the striatum in PSP. The lack of correlation between DVR-max and FDG uptake supports this view. Thus, striatal D2R status and cerebral glucose metabolism likely represent independent disease markers in PSP