Syrimi Zoe Joanna, Vojtisek Lubomir, Eliasova Ilona, Viskova Jana, Svatkova Alena, Vanicek Jiri, Rektorova Irena
Medical Faculty, Masaryk University, Brno, Czech Republic.
Multimodal and Functional Neuroimaging Research Group, CEITEC-Central European Institute of Technology, Masaryk University, Brno, Czech Republic.
J Neural Transm (Vienna). 2017 May;124(5):551-557. doi: 10.1007/s00702-017-1703-1. Epub 2017 Mar 7.
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.
虽然先前的研究表明帕金森病(PD)中的灌注异常是由痴呆症驱动的,但我们的研究旨在确定非痴呆PD患者认知改变的灌注基础。使用动脉自旋标记(ASL)测量了28例PD患者(年龄65岁±9.9标准差)和16例年龄匹配的健康对照者(HC)(年龄65岁±7.8标准差)的脑血流量,这些患者和对照者还接受了神经学和认知测试。使用SPM8软件对22例PD患者和16例HC的三维伪连续ASL和T2加权扫描进行了体素分析。通过Spearman相关分析评估感兴趣区(VOI)的ASL值与行为和认知测量之间的关联。与HC相比,PD患者在左侧缘上回/颞上回(VOI1)和左侧后扣带回/楔前叶(VOI2)存在后皮质灌注不足。在排除年龄、左旋多巴等效剂量(LED)和总颅内体积(TIV)的影响后,发现VOI2中的灌注与修订后的Addenbrooke认知检查(ACE-R)评分呈正相关(R = 0.51,p = 0.04)。相反,在排除运动障碍、年龄、LED和TIV的影响后,检测到VOI1与ACE-R之间呈负相关(R = -0.62,p = 0.01)。在非痴呆的PD患者中,楔前叶/后扣带回的血流异常与运动障碍水平和整体认知表现相关。相反,缘上回的灌注异常可能是大脑退化和认知表现下降的一种代偿机制。