Arterial spin labelling detects posterior cortical hypoperfusion in non-demented patients with Parkinson's disease
| Autoři | |
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| Rok publikování | 2017 |
| Druh | Článek v odborném periodiku |
| Časopis / Zdroj | Journal of Neural Transmission |
| Fakulta / Pracoviště MU | |
| Citace | |
| Doi | http://dx.doi.org/10.1007/s00702-017-1703-1 |
| Klíčová slova | Parkinson's disease; Arterial spin labelling; Perfusion; Cognitive performance |
| Popis | While previous studies suggested that perfusion abnormalities in Parkinson's disease (PD) are driven by dementia, our study aimed to identify perfusion underpinning of cognitive alteration in non-demented PD patients. Cerebral blood flow was measured using arterial spin labelling (ASL) in 28 PD patients (age 65 years +/- 9.9 SD) and 16 age-matched healthy controls (HC) (age 65 years +/- 7.8 SD), who also underwent neurological and cognitive testing. The 3D pseudocontinuous ASL and T2-weighted scans from 22 PD patients and 16 HC were analysed in a voxel-wise manner using SPM8 software. Associations between the ASL values in volumes of interest (VOIs) and behavioural and cognitive measures were assessed by Spearman correlation analysis. Posterior cortical hypoperfusion was found in PD patients compared to HC in the left supramarginal gyrus/superior temporal gyrus (VOI1) and left posterior cingulate/precuneus (VOI2). Positive correlation was revealed between perfusion in the VOI2 and Addenbrooke's Cognitive Examination Revised (ACE-R) scores after filtering out the effect of age, levodopa equivalent dose (LED), and total intracranial volume (TIV) (R = 0.51, p = 0.04). Conversely, negative correlation between VOI1 and ACE-R was detected (R = -0.62, p = 0.01) after regressing out the effects of motor impairment, age, LED, and TIV. In non-demented subjects with PD, blood flow abnormalities in precuneus/posterior cingulate were linked to the level of motor impairment and global cognitive performance. Oppositely, perfusion abnormalities in supramarginal gyrus might serve as a compensatory mechanism for brain degeneration and decreased cognitive performance. |
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