Evidence for cortical dysfunction in clinically non-demented patients with Parkinson’s disease: a proton MR spectroscopy study
- M T M Hua,b,c,
- S D Taylor-Robinsona,
- K Ray Chaudhuric,
- J D Bella,
- R G Morrisc,
- C Cloughc,
- D J Brooksb,
- N Turjanskib
- aRobert Steiner MR Unit, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK, bMedical Research Council Cyclotron Unit, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Rd, London W12 0NN, UK, cKing’s College Hospital Medical School and Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, UK
- Dr M T M Hu, Medical Research Council Cyclotron Unit, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Rd, London W12 0NN, UK. Telephone 0181 383 3710; Fax 0181 383 2029.
- Received 12 October 1998
- Revised 8 February 1999
- Accepted 16 February 1999
Abstract
OBJECTIVES To investigate whether proton magnetic resonance spectroscopy (1H MRS) can detect cortical dysfunction in non-demented patients with Parkinson’s disease, and to correlate changes with cognitive function on formal neuropsychological testing.
METHODS Multivoxel1H MRS was performed in 17 patients with levodopa treated idiopathic Parkinson’s disease with out clinical dementia, and 10 age match ed control subjects. Measurements of N-acetylaspartate (NAA)/choline (Cho), NAA/creatine+phosphocreatine (Cr), and Cho/Cr were obtained from right and left temporoparietal cortex and occipital cortex. Fourteen patients with Parkinson’s disease underwent a full battery of neuropsychological testing including performance and verbal subtests of the WAIS-R, Boston naming test, FAS test, and California verbal learning test.
RESULTS There were significant temporoparietal cortex reductions in NAA/Cr ratios in right and left averaged spectra of the patients with Parkinson’s disease (p=0.012 after Bonferroni correction) and in spectra contralateral to the worst clinically affected limbs of the patients with Parkinson’s disease compared with controls (p = 0.003 after Bonferroni correction). There was a significant correlation between reduction in NAA/Cr ratios and measures of global cognitive decline, occurring independently of motor impairment (p=0.019).
CONCLUSIONS This study suggests that 1H MRS can detect temporoparietal cortical dysfunction in non-demented patients with Parkinson’s disease. Further longitudinal studies are needed to investigate whether these1H MRS changes are predictive of future cognitive impairment in the subset of patients with Parkinson’s disease who go on to develop dementia, or occur as part of the normal Parkinson’s disease process.
