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July 1990

Positron Emission Tomography Study in Progressive Supranuclear Palsy: Brain Hypometabolic Pattern and Clinicometabolic Correlations

Author Affiliations

From the Service Hospitalier Frederic Joliot, CEA, Departement de Biologie, Hopital d'Orsay (France) (Drs Blin, Baron, and Cambon); the Clinique de Neurologie et Neuropsychologie and Institut National de la Santé et de la Recherche Medicale U289, Hopital de la Salpêtrière, Paris, France (Drs Dubois, Pillon, and Agid); the Service de Neurologie, Hopital Beaujon, Clichy (France) (Dr Cambier); and the Institut National de la Santé et de la Recherche Medicale, U320, Caen, France (Dr Baron).

Arch Neurol. 1990;47(7):747-752. doi:10.1001/archneur.1990.00530070035009

• In 41 patients with progressive supranuclear palsy (PSP) that was diagnosed on the basis of eight clinical criteria (25 patients with all eight criteria [probable PSP] and 16 with six or seven criteria [possible PSP]), we studied cerebral energy metabolism by using positron emission tomography and the fludeoxyglucose F 18 or the oxygen 15 method. Compared with age-matched controls, each of the cortical and subcortical metabolic values was significantly reduced, with a predominance in the frontal cortex, in both groups of patients with probable and possible PSP, without a difference between these two groups, suggesting similar underlying disease. The frontal metabolic value decreased with disease duration, but the relative frontal hypometabolism (expressed as the fronto-occipital metabolic ratio) was apparently already present in the early stages of the disease. The parkinsonian motor score was correlated with the caudate and thalamic metabolic values. The intellectual deterioration index was significantly correlated with both the frontal and the nonfrontal metabolic values. Finally, the frontal neuropsychological score was significantly correlated with only the fronto-occipital metabolic ratio. Hence, in PSP, a degenerative brain disease with subcortical lesions, the prominent frontal lobe-like syndrome essentially depends on the relative hypometabolism of the frontal cortex.

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