SEPARATING PARKINSONS-DISEASE FROM NORMALITY - DISCRIMINANT FUNCTION-ANALYSIS OF FLUORODOPA F-18 POSITRON EMISSION TOMOGRAPHY DATA

Citation
Gv. Sawle et al., SEPARATING PARKINSONS-DISEASE FROM NORMALITY - DISCRIMINANT FUNCTION-ANALYSIS OF FLUORODOPA F-18 POSITRON EMISSION TOMOGRAPHY DATA, Archives of neurology, 51(3), 1994, pp. 237-243
Citations number
29
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
51
Issue
3
Year of publication
1994
Pages
237 - 243
Database
ISI
SICI code
0003-9942(1994)51:3<237:SPFN-D>2.0.ZU;2-S
Abstract
Objective: To explore the relationship between normal and parkinsonian fluorodopa F 18 (F-18-6-L-fluorodopa [F-18-dopa]) uptake data to iden tify clinically normal subjects who may have preclinical Parkinson's d isease. Design: A statistical comparison of striatal fluorodopa F 18 p ositron emission tomography scan data from patients with Parkinson's d isease and normal controls. Setting: Positron mission tomography unit within a postgraduate teaching hospital. Main Outcome Measures: Discri minant function analysis used to compare the pattern of striatal (left and right caudate and putamen) fluorodopa F 18 uptake in normal subje cts and patients with Parkinson's disease. Results: The discriminant s core that best separates patients with Parkinson's disease from normal controls is a function of the lowest putamen influx constant minus a function of the caudate influx constant values. Borderline low normal subjects have slightly low fluorodopa F 18 uptake throughout the stria tum,whereas patients with early Parkinson's disease have low fluorodop a F 18 uptake in one putamen with preserved uptake in the caudate (for normal subjects, subtracting the caudate influx constants from a func tion of the lowest putamen value lowers the discriminant score, althou gh it remains positive; for patients, subtracting a larger caudate val ue from a function of the putamen uptake Value leads to a negative sco re). One control subject had a borderline low discriminant score, comp atible with focal nigral pathological changes as expected in preclinic al Parkinson's disease. A repeated scan taken 3 years later showed a m arked reduction in fluorodopa F 18 uptake, suggesting progressive nigr al dysfunction. Conclusion: Normal and parkinsonian fluorodopa F 18 up take data differ both in the overall level of tracer uptake and in its spatial distribution. Subjects whose overall striatal fluorodopa F 18 uptake falls at the borderline of normal and parkinsonian values are likely to be normal if they have uniformly low uptake, but may have ea rly or preclinical Parkinson's disease if uptake into putamen is very much lower than uptake into caudate.