4.7 Article

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

Journal

BRAIN
Volume 123, Issue -, Pages 340-352

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/brain/123.2.340

Keywords

Parkinson's disease; magnetic resonance spectroscopy; PET; glucose; dementia

Funding

  1. MRC [MC_U120061305] Funding Source: UKRI
  2. Medical Research Council [MC_U120061305] Funding Source: researchfish
  3. Medical Research Council [MC_U120061305] Funding Source: Medline

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Regional cerebral phosphorus-31 magnetic resonance spectroscopy (P-31-MRS) was performed in 10 nondemented Parkinson's disease patients and nine age-matched 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 underwent neuropsychological testing including performance and verbal subtests of the Wechsler Adult Intelligence Scale-Revised, Boston Naming Test, Controlled 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 ganglia and brainstem were obtained. P-31 MR peak area ratios of signals from phosphomonoesters (PMEs), inorganic phosphate (P-i), phosphodiesters (PDEs), alpha-ATP, gamma-ATP and phosphocreatine (PCr) relative to beta-ATP were measured. Relative percentage peak areas of PMEs, P-i, PDEs, PCr, and alpha-, beta- and gamma-ATP signals were also measured with respect to the total P-31-MRS signal. Significant bilateral increases in the P-i/beta-ATP ratio 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 controls. In the right temporoparietal cortex, there was also a significant increase in the mean relative percentage P-i (P = 0.001). (18)FDG-PET revealed 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, using both volume of interest analysis and statistical parametric mapping. There were significant correlations between right temporoparietal P-i/beta-ATP 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 summary, temporoparietal cortical hypometabolism was seen in non-demented Parkinson's disease patients with both P-31-MRS and (18)FDG-PET, suggesting that both glycolytic and oxidative pathways are impaired. This dysfunction may reflect either the presence of primary cortical pathology or deafferentation of striato-cortical projections. P-31-MRS and (18)FDG-PET may both provide useful predictors of future cognitive impairment in a subset of Parkinson's disease patients who go on to develop dementia.

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