title: PET evaluation of the relationship between D2 receptor binding and glucose metabolism in patients with parkinsonism.
abstract: OBJECTIVE
  To clarify the relationship between D2 receptor binding and the cerebral metabolic rate for glucose (CMRGlu) in patients with parkinsonism, we simultaneously measured both of these factors, and then compared the results.
  
  
  METHODS
  The subjects consisted of 24 patients: 9 with Parkinson's disease (PD), 3 with Juvenile Parkinson's disease (JPD), 9 with multiple system atrophy (MSA), and 3 with progressive supranuclear palsy (PSP). The striatal D2 receptor binding was measured by the C-11 raclopride transient equilibrium method. CMRGlu was investigated by the F-18 fluorodeoxyglucose autoradiographic method.
  
  
  RESULTS
  The D2 receptor binding in both the caudate nucleus and putamen showed a positive correlation with the CMRGlu in the PD-JPD group, but the two parameters demonstrated no correlation in the MSA-PSP group. The left/right (L/R) ratio of D2 receptor binding in the putamen showed a positive correlation with that of CMRGlu in the MSA-PSP group, while the two demonsrated no correlation in the PD-JPD group.
  
  
  CONCLUSIONS
  Our PET study showed striatal D2 receptor binding and the CMRGlu to be closely related in patients with parkinsonism, even though the results obtained using the L/R ratios tended to differ substantially from those obtained using absolute values. The reason for this difference is not clear, but this finding may reflect the pathophysiology of these disease entities.
authors.affiliation: Department of Radiology, Fukuoka Red Cross Hospital, 3-1-1 Ookusu, Minami-ku, Fukuoka 815-8555, Japan. nanchan-kyu@umin.ac.jp
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakagawa
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kuwabara
authors.forename: Takayuki
authors.initials: T
authors.lastname: Taniwaki
authors.forename: Masayuki
authors.initials: M
authors.lastname: Sasaki
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Koga
authors.forename: Koichiro
authors.initials: K
authors.lastname: Kaneko
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Hayashi
authors.forename: Jun-ichi
authors.initials: J
authors.lastname: Kira
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Honda
mesh_terms: D000328:Adult; D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D001921:Brain / Q000000981:diagnostic imaging* / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000493:pharmacokinetics; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000378:metabolism*; D049268:Positron-Emission Tomography / Q000379:methods*; D020891:Raclopride / Q000493:pharmacokinetics; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D017448:Receptors, Dopamine D2 / Q000378:metabolism*; D014018:Tissue Distribution / Q000187:drug effects
chemical_list: D000978:Antiparkinson Agents; D019275:Radiopharmaceuticals; D017448:Receptors, Dopamine D2; D019788:Fluorodeoxyglucose F18; D020891:Raclopride; D007980:Levodopa; D005947:Glucose