title: Functional effects of striatal dysfunction in Parkinson disease.
abstract: BACKGROUND
  Concepts of basal ganglia organization suggest structually and functionally segregated pathways that link putamen and caudate function to motor and cognitive performance, respectively.
  
  
  OBJECTIVE
  To investigate whether motor and cognitive impairment in Parkinson disease is attributable to selective disturbance in nigrostriatal, dopaminergic function and regional cerebral glucose metabolism.
  
  
  METHODS
  Twenty patients with probable Parkinson disease underwent positron emission tomographic measurements of dopaminergic, nigrostriatal function (positron emission tomography with fluorodopa F 18), regional glucose metabolism (positron emission tomography with fludeoxyglucose F 18), memory testing, and evaluation of locomotor disability.
  
  
  RESULTS
  Memory performance in the patient cohort strongly correlated with the individual disease duration and degree of locomotor disability (P < .05). Striatal uptake rates of fluorodopa F 18 were significantly reduced in all patients (P < .05) compared with those in normal control subjects, and putaminal rates correlated significantly with the patients' degree of locomotor disability (P < .01) but not with memory performance. In the patients with an advanced stage of disease, there was a significant correlation between reduced caudate uptake rates of fluorodopa F 18 and the patients' impairment in delayed recall performance of the memory task (P < .05) but not with the individual degree of locomotor disability. No changes were found for regional glucose metabolic rates in the patients compared with the controls.
  
  
  CONCLUSIONS
  The present study provides evidence for the hypothesis that on the level of the striatum, motor impairment in Parkinson disease may be assigned to altered dopamine neuronal integrity in the putamen but not in the caudate, whereas memory impairment in the more advanced cases may be attributed to caudate but not putaminal dysfunction.
authors.affiliation: Max-Planck-Institut für Neurologische Forschung, Köln, Germany.
authors.forename: V A
authors.initials: VA
authors.lastname: Holthoff-Detto
authors.forename: J
authors.initials: J
authors.lastname: Kessler
authors.forename: K
authors.initials: K
authors.lastname: Herholz
authors.forename: H
authors.initials: H
authors.lastname: Bönner
authors.forename: U
authors.initials: U
authors.lastname: Pietrzyk
authors.forename: M
authors.initials: M
authors.lastname: Würker
authors.forename: M
authors.initials: M
authors.lastname: Ghaemi
authors.forename: K
authors.initials: K
authors.lastname: Wienhard
authors.forename: R
authors.initials: R
authors.lastname: Wagner
authors.forename: W D
authors.initials: WD
authors.lastname: Heiss
mesh_terms: D000368:Aged; D001479:Basal Ganglia / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D003342:Corpus Striatum / Q000503:physiopathology; D003847:Deoxyglucose / Q000031:analogs & derivatives; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008297:Male; D008568:Memory; D008875:Middle Aged; D009068:Movement; D010300:Parkinson Disease / Q000378:metabolism / Q000503:physiopathology*; D011877:Radionuclide Imaging
chemical_list: D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005947:Glucose