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
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.