Fluorodeoxyglucose positron emission tomography in Richardson's syndrome and progressive supranuclear palsy‐parkinsonism

Abstract

We hypothesized that postural instability and cognitive decline in patients with Richardson’s syndrome could be a consequence of reduced thalamic and frontal metabolism. Severe Parkinsonian signs in patients with progressive supranuclear palsy-parkinsonism may be reflected by alterations in putaminal metabolism. Eleven patients with Richardson’s syndrome, 8 patients with progressive supranuclear palsy-parkinsonism, 12 with Parkinson’s disease, and 10 controls underwent clinical assessment and fluorodeoxyglucose positron emission tomography (PET). Richardson’s syndrome patients showed pronounced thalamic hypometabolism, and patients with progressive supranuclear palsy-parkinsonism pronounced putaminal hypometabolism, compared to all other investigated groups. The putamen/thalamus uptake ratio differentiated progressive supranuclear palsy-parkinsonism from Richardson’s syndrome (area under the curve 5 0.86) and from Parkinson’s disease (area under the curve 5 0.80) with acceptable accuracy. Frontal hypometabolism was predominantly found in Richardson’s syndrome patients. Richardson’s syndrome, progressive supranuclear palsy-parkinsonism and Parkinson’s disease showed different metabolic patterns in fluorodeoxyglucose PET.