Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease.

The differentiation between progressive supranuclear palsy (PSP) and Parkinson's disease (PD) may be difficult, especially in the early stages of disease. Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F-fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested.

Is FDG-PET a useful tool in clinical practice for diagnosing corticobasal ganglionic degeneration?

Seven consecutive patients were suspected to suffer from corticobasal ganglionic degeneration (CBGD) and were studied with ([18])F-fluorodeoxyglucose (FDG) PET imaging of the brain. At the time of their FDG-PET scan, 4 of 7 patients fulfilled the clinical criteria of CBGD as proposed by Lang and associates [In Calne DB, 1994; Neurodegenerative disease. Philadelphia: Saunders]. For 2 of these 4 patients, however, an alternative clinical diagnosis was also considered. Three of the seven patients underwent an FDG-PET scan when their clinical features were not yet developed sufficiently to confirm a clinical diagnosis of CBGD. Simple visual analysis of the FDG-PET scans was carried out. All 7 patients showed an asymmetrical pattern of glucose metabolism that was demonstrated in previous studies to be characteristic in patients who had a clinical diagnosis of CBGD. The PET results helped to confirm the clinical suspicion of CBGD in 2 patients and to rule out other diagnoses in 2 other patients. For 3 patients with no sufficient symptoms to diagnose CBGD, the pattern of glucose metabolism was characteristically asymmetrical. A probable diagnosis of CBGD was made in these patients. Our results suggest that routine visual inspection of a cerebral FDG-PET scan is a useful tool to confirm suspicion of the clinical diagnosis of probable CBGD, to differentiate from other hypokinetic-rigid syndromes, and to support a diagnosis CBGD in patients who do not (yet) sufficiently fulfill the clinical criteria.