FUNCTIONAL-EFFECTS OF STRIATAL DYSFUNCTION IN PARKINSON DISEASE

Background: Concepts of basal ganglia organization suggest structually and functionally segregated pathways that link putamen and caudate fu nction to motor and cognitive performance, respectively. Objective: To investigate whether motor and cognitive impairment in Parkinson disea se is attributable to selective disturbance in nigrostriatal, dopamine rgic function and regional cerebral glucose metabolism. Design: Twenty patients with probable Parkinson disease underwent positron emission tomographic measurements of dopaminergic, nigrostriatal function (posi tron emission tomography with fluorodopa F 18), regional glucose metab olism (positron emission tomography with fludeoxyglucose F 18), memory testing, and evaluation of locomotor disability. Results: Memory perf ormance in the patient cohort strongly correlated with the individual disease duration and degree of locomotor disability (P < .05). Striata l uptake rates of fluorodopa F 18 were significantly reduced in all pa tients (P < .05) compared with those in normal control subjects, and p utaminal rates correlated significantly with the patients' degree of l ocomotor disability (P < .01) but not with memory performance. In the patients with an advanced stage of disease, there was a significant co rrelation between reduced caudate uptake rates of fluorodopa F 18 and the patients' impairment in delayed recall performance of the memory t ask (P < .05) but not with the individual degree of locomotor disabili ty. No changes were found for regional glucose metabolic rates in the patients compared with the controls. Conclusions: The present study pr ovides evidence for the hypothesis that on the level of the striatum, motor impairment in Parkinson disease may be assigned to altered dopam ine neuronal integrity in the putamen but not in the caudate, whereas memory impairment in the more advanced cases may be attributed to caud ate but not putaminal dysfunction.