title: Glucose metabolism in small subcortical structures in Parkinson's disease.
abstract: OBJECTIVE
  Evidence from experimental animal models of Parkinson's disease (PD) suggests a characteristic pattern of metabolic perturbation in discrete, very small basal ganglia structures. These structures are generally too small to allow valid investigation by conventional positron emission tomography (PET) cameras. However, the high-resolution research tomograph (HRRT) PET system has a resolution of 2 mm, sufficient for the investigation of important structures such as the pallidum and thalamic subnuclei.
  
  
  METHODS
  Using the HRRT, we performed [(18)F]-fluorodeoxyglucose (FDG) scans on 21 patients with PD and 11 age-matched controls. We employed three types of normalization: white matter, global mean, and data-driven normalization. We performed volume-of-interest analyses of small subcortical gray matter structures. Voxel-based comparisons were performed to investigate the extent of cortical hypometabolism.
  
  
  RESULTS
  The most significant level of relative subcortical hypermetabolism was detected in the external pallidum (GPe), irrespective of normalization strategy. Hypermetabolism was suggested also in the internal pallidum, thalamic subnuclei, and the putamen. Widespread cortical hypometabolism was seen in a pattern very similar to previously reported patterns in patients with PD.
  
  
  CONCLUSIONS
  The presence and extent of subcortical hypermetabolism in PD is dependent on type of normalization. However, the present findings suggest that PD, in addition to widespread cortical hypometabolism, is probably characterized by true hypermetabolism in the GPe. This finding was predicted by the animal 2-deoxyglucose autoradiography literature, in which high-magnitude hypermetabolism was also most robustly detected in the GPe.
authors.affiliation: PET Centre, Aarhus University Hospitals, Denmark. per@pet.auh.dk
authors.forename: Per
authors.initials: P
authors.lastname: Borghammer
authors.forename: Søren B
authors.initials: SB
authors.lastname: Hansen
authors.forename: Carsten
authors.initials: C
authors.lastname: Eggers
authors.forename: Mallar
authors.initials: M
authors.lastname: Chakravarty
authors.forename: Kim
authors.initials: K
authors.lastname: Vang
authors.forename: Joel
authors.initials: J
authors.lastname: Aanerud
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Hilker
authors.forename: Wolf-Dieter
authors.initials: WD
authors.lastname: Heiss
authors.forename: Anders
authors.initials: A
authors.lastname: Rodell
authors.forename: Ole L
authors.initials: OL
authors.lastname: Munk
authors.forename: David
authors.initials: D
authors.lastname: Keator
authors.forename: Albert
authors.initials: A
authors.lastname: Gjedde
mesh_terms: D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging* / Q000378:metabolism* / Q000503:physiopathology; D001928:Brain Diseases, Metabolic / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000503:physiopathology; D016022:Case-Control Studies; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000000981:diagnostic imaging* / Q000378:metabolism / Q000503:physiopathology; D049268:Positron-Emission Tomography / Q000379:methods* / Q000592:standards
chemical_list: D005947:Glucose