The effect of age and disease duration on cerebral glucose metabolism in patients with Parkinson's disease

Abstract

[한글]

[영문]Background: Although the core pathology of Parkinson’s disease (PD) is the uniform dopaminergic cell loss in the substantia nigra, the clinical features are markedly diverse. Neuronal degenerations associated with PD itself and in aging may affect the evolution of PD in additive or augmentative manner. Those degenerations also have been focused to explain the clinical diversity. However, no systematic study has been reported on the clinical deficits and topography of dysfunctional brain areas correlating with the age of patients and duration of disease, respectively. Methods: The present study included 128 non-demented PD patients. The severity of parkinsonian motor deficit was measured using unified Parkinson’s disease rating scale (UPDRS) motor scores. All underwent brain magnetic resonance imaging and [18F]-fluorodeoxy glucose positron emission tomography studies. Multiple linear regression analysis was used to find parkinsonian motor deficits of which severity correlate with the age of patients and severity correlate with the disease duration. A multiple regression model was used to find brain areas in which cerebral glucose metabolism (CMRglu) correlates with age of patients and disease duration. Results: The mean (SD) age of patients was 64.6 (8.1) years and the mean of disease duration was 49.3 (49.7) months. The mean of total UPDRS motor score was 28 (13.6). Mean UPDRS motor score of the severity of tremor was 3.6 (3.3), rigidity was 5.3 (3.7), bradykinesia was 9.5 (4.5) and axial symptoms was 4.3 (3.2). The age of patients correlated positively with total UPDRS motor scores. It also correlated with the severity of bradykinesia and axial motor deficits, but not with that of tremor and rigidity. The disease duration correlated with the total UPDRS and all four UPDRS subscores representing tremor, rigidity, bradykinesia, and axial mtor deficit. The age of patients correlated inversely with the regional glucose metabolism of the prefrontal, orbitofrontal, superior temporal, anterior and posterior cingulate cortices, parahippocampal gyrus, caudate and thalamus. In contrast, disease duration correlated inversely with the metabolism of occipital cortex. Conclusions: In PD, age and disease duration have independent, additive effects on the deterioration of cortical metabolism, which leads to various clinical disabilities in PD patients. Moreover, age-related widespread, particularly frontal, dysfunction may accelerate deterioration of bradykinesia and axial motor deficits.