REGIONAL HYPOMETABOLISM IN ALZHEIMERS-DISEASE AS MEASURED BY POSITRONEMISSION TOMOGRAPHY AFTER CORRECTION FOR EFFECTS OF PARTIAL VOLUME AVERAGING

Citation
Cc. Meltzer et al., REGIONAL HYPOMETABOLISM IN ALZHEIMERS-DISEASE AS MEASURED BY POSITRONEMISSION TOMOGRAPHY AFTER CORRECTION FOR EFFECTS OF PARTIAL VOLUME AVERAGING, Neurology, 47(2), 1996, pp. 454-461
Citations number
60
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
47
Issue
2
Year of publication
1996
Pages
454 - 461
Database
ISI
SICI code
0028-3878(1996)47:2<454:RHIAAM>2.0.ZU;2-P
Abstract
Measurements of cerebral metabolism in patients with Alzheimer's disea se (AD) using PET are artifactually depressed due to partial volume av eraging of brain tissue activity with enlarged CSF spaces. To investig ate the effects of correction for the expansion of CSF spaces on regio nal metabolic measures, as well as the correlations between neuropsych ological test results and resting cerebral metabolism before and after partial volume correction, we applied an MRI-based method of partial volume correction to F-18-fluorodeoxyglucose (FDG)-PET data from eight patients diagnosed with probable AD and ten healthy elderly individua ls. Before correction, the AD group had significantly lower cortex-to- cerebellum ratios in the posterior temporal, parietal, and frontal lob es in comparison to the control subjects. Partial volume correction of PET data resulted in 19 to 49% increases in regional activity in the AD group and 16 to 38% increases in the control group. The patients' p ersistence of significant hypometabolism in the frontal, posterior tem poral, and parietal regions after partial volume correction suggests t hat a. true reduction in regional cerebral glucose metabolism occurs i n AD, even though its magnitude is a result of both metabolic reductio ns and the effects of atrophy. Partial volume correction of PET data i n the AD group had a significant impact on the correlations between re gional glucose metabolism and neuropsychological performance. These fi ndings suggest that accounting for differential extent and distributio n of cerebral atrophy in patients with AD and in healthy individuals m ay potentially improve our ability to interpret specific cognitive dys function in the context of the functional imaging data.