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The correlation between cerebral glucose metabolism and benzodiazepine receptor density in the acute vegetative state

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Rudolf,  Jobst
Klinisches PET, Neurologische Abteilung, Max-Planck-Institut für neurologische Forschung, Managing Director: D. Yves von Cramon, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Sobesky,  Jan
Klinisches PET, Neurologische Abteilung, Max-Planck-Institut für neurologische Forschung, Managing Director: D. Yves von Cramon, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Ghaemi,  Mehran
Wolf-Dieter Heiss, Emeriti, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Heiss,  Wolf-Dieter
Wolf-Dieter Heiss, Emeriti, Max Planck Institute for Metabolism Research, Managing Director: Jens Brüning, Max Planck Society;

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Citation

Rudolf, J., Sobesky, J., Ghaemi, M., & Heiss, W.-D. (2002). The correlation between cerebral glucose metabolism and benzodiazepine receptor density in the acute vegetative state. European Journal of Neurology, 9(6), 671-677.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0026-D9D6-E
Abstract
This paper compares the results of parallel positron emission tomography ( PET) studies of regional cerebral glucose metabolism with the radiotracer F-18-fluorodeoxyglucose (FDG) and benzodiazepine receptor (BZR) density by PET using the BZR ligand C-11-flumazenil (FMZ), a tracer of neuronal integrity, in nine patients with acute vegetative state (AVS, duration <1 month). Overall glucose utilization was significantly reduced in AVS in comparison with age-matched controls (global metabolic rate for glucose 26 μmol/100 g/min in AVS vs. 31 μmol/100g/min in controls). FMZ-PET demonstrated a considerable reduction of BZR binding sites in all cortical regions that grossly corresponded to the extent of reduction of cerebral glucose metabolism assessed with FDG-PET, whilst the cerebellum was spared from neuronal loss. In controls, cortical relative flumazenil binding was not lower than five times the average white matter activity, whilst in AVS, nearly all values were below this threshold. There was no relevant overlap of the data of relative umazenil binding between both groups. The comparison of FDG- and FMZ-PET findings in AVS demonstrates that alterations of cerebral glucose consumption do not represent mere functional inactivation, but irreversible structural brain damage.