Cortical dysfunction in non-demented Parkinson's disease patients - A combined P-31-MRS and (18)FDG-PET study

Citation
Mtm. Hu et al., Cortical dysfunction in non-demented Parkinson's disease patients - A combined P-31-MRS and (18)FDG-PET study, BRAIN, 123, 2000, pp. 340-352
Citations number
63
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
123
Year of publication
2000
Part
2
Pages
340 - 352
Database
ISI
SICI code
0006-8950(200002)123:<340:CDINPD>2.0.ZU;2-H
Abstract
Regional cerebral phosphorus-31 magnetic resonance spectroscopy (P-31-MRS) was performed in 10 nondemented Parkinson's disease patients and nine age-m atched control subjects. Five of the patients undergoing P-31-MRS and four additional Parkinson's disease patients had cerebral 2-[F-18]fluoro-2-deoxy -D-glucose PET ((18)FDG-PET), the results of which were compared with those of eight age-matched control subjects. All Parkinson's disease patients un derwent neuropsychological testing including performance and verbal subtest s of the Wechsler Adult Intelligence Scale-Revised, Boston Naming Test, Con trolled Oral World Association test (FAS Test) and California Learning Test to exclude clinical dementia. P-31 MR spectra from right and left temporo- parietal cortex, occipital cortex and a central voxel incorporating basal g anglia and brainstem were obtained. P-31 MR peak area ratios of signals fro m phosphomonoesters (PMEs), inorganic phosphate (P-i), phosphodiesters (PDE s), alpha-ATP, gamma-ATP and phosphocreatine (PCr) relative to beta-ATP wer e measured. Relative percentage peak areas of PMEs, P-i, PDEs, PCr, and alp ha-, beta- and gamma-ATP signals were also measured with respect to the tot al P-31-MRS signal. Significant bilateral increases in the P-i/beta-ATP rat io were found in temporoparietal cortex (P = 0.002 right and P = 0.014 left cortex) for the non-demented Parkinson's disease patients compared with co ntrols. In the right temporoparietal cortex, there was also a significant i ncrease in the mean relative percentage P-i (P = 0.001). (18)FDG-PET reveal ed absolute bilateral reductions in glucose metabolism after partial volume effect correction in posterior parietal and temporal cortical grey matter (P < 0.01 and P < 0.05, respectively) for the Parkinson's disease group, us ing both volume of interest analysis and statistical parametric mapping. Th ere were significant correlations between right temporoparietal P-i/beta-AT P ratios and estimated reductions in performance IQ (r = 0.96, P < 0.001). Left temporoparietal P-i/beta-ATP ratios correlated with full scale IQ and verbal IQ (r = - 0.82, P = 0.006, r = -0.86, P = 0.003, respectively), In s ummary, temporoparietal cortical hypometabolism was seen in non-demented Pa rkinson's disease patients with both P-31-MRS and (18)FDG-PET, suggesting t hat both glycolytic and oxidative pathways are impaired. This dysfunction m ay reflect either the presence of primary cortical pathology or deafferenta tion of striato-cortical projections. P-31-MRS and (18)FDG-PET may both pro vide useful predictors of future cognitive impairment in a subset of Parkin son's disease patients who go on to develop dementia.