Division of Nuclear Medicine, Department of Radiology, University of Michigan, Ann Arbor, Michigan 48109-0028, USA.
J Nucl Med. 2011 Jun;52(6):848-55. doi: 10.2967/jnumed.111.089946. Epub 2011 May 13.
Longitudinal studies in nondemented Parkinson disease (PD) subjects offer an opportunity to study the earliest regional cerebral subcortical and cortical metabolic changes underlying incident dementia in this disorder.
Twenty-three PD subjects without dementia (Hoehn and Yahr stages I-III; age, 61.8 ± 9.7 y; Mini-Mental State Examination, 28.0 ± 1.4) and 27 controls (age, 59.8 ± 11.5 y) underwent (18)F-FDG PET at study entry. PD subjects underwent yearly clinical assessment to determine conversion to dementia. The mean duration of follow-up was 3.9 ± 1.2 y (range, 2.0-6.8 y). Follow-up (18)F-FDG PET was available in a subset of subjects at 2 or more years. Both volume-of-interest and 3-dimensional stereotactic surface projection (3D-SSP) analyses were performed.
Six subjects became demented (PDD), with a mean time of 3.8 ± 1.7 y (range, 1.9-6.0 y) to development of dementia. Mean duration of disease before onset of dementia was 9.7 ± 4.2 y (range, 3.1-14 y). There were significant metabolic reductions in the occipital (-11.8% vs. controls, F((2,22)) = 7.0, P = 0.002) and posterior cingulate (-12.1% vs. controls, F((2,22)) = 5.2, P = 0.009) cortices in PDD subjects at baseline, before diagnosis of dementia, compared with controls. Metabolism was most diminished in the visual association cortex (Brodmann area [BA] 18; -20.0% vs. control, F((2,22)) = 8.45, P = 0.0007) of PDD subjects. There was mild hypometabolism in the caudate nucleus (-8.4% vs. control, F((2,22)) = 3.2, P < 0.05). There was no significant hypometabolism in the temporal or frontal lobes. PD subjects who did not become demented (non-PDD), compared with controls, had reduced cerebral metabolism in the primary occipital cortex (BA 17) that was revealed only by 3D-SSP analysis. Follow-up scans in 5 PDD subjects at 2 y after study entry demonstrated a significant interval within-subject change in the thalamus (-11.4%), posterior cingulate (-9%), occipital (-7%), parietal (-7%), and frontal cortices (-7%) and mild reductions in the temporal cortex (-5%) and hippocampus (-3%), compared with study entry scans.
Incident dementia in idiopathic PD is heralded by decreased metabolism in the visual association (BA 18) and posterior cingulate cortices, with mild involvement also of the caudate nucleus. Two-year follow-up data from 5 PDD converters show that progression to dementia is associated with mixed subcortical and cortical changes that involve the mesiofrontal lobes also. These findings provide insights into early metabolic features of parkinsonian dementia.
在非痴呆帕金森病（PD）患者的纵向研究中，有机会研究该疾病中发生痴呆的潜在认知障碍的早期大脑皮质下和皮质代谢变化。
23 名无痴呆（Hoehn 和 Yahr 分期 I-III；年龄 61.8 ± 9.7 岁；简易精神状态检查 28.0 ± 1.4）和 27 名对照者（年龄 59.8 ± 11.5 岁）在研究开始时接受了（18）F-FDG PET。PD 患者每年进行临床评估以确定是否转化为痴呆。平均随访时间为 3.9 ± 1.2 年（范围 2.0-6.8 年）。在一些患者中，可获得随访 2 年以上的（18）F-FDG PET 扫描。进行了基于感兴趣区和三维立体定向表面投影（3D-SSP）的分析。
6 名患者出现痴呆（PDD），从出现痴呆到发病的平均时间为 3.8 ± 1.7 年（范围 1.9-6.0 年）。在痴呆发病前，疾病的平均病程为 9.7 ± 4.2 年（范围 3.1-14 年）。与对照组相比，基线时（即在诊断为痴呆之前）PDD 患者的枕叶（-11.8%，与对照组相比，F（2,22）=7.0，P=0.002）和后扣带回（-12.1%，与对照组相比，F（2,22）=5.2，P=0.009）皮质代谢明显降低。PDD 患者的视觉联合皮质（Brodmann 区 18；-20.0%，与对照组相比，F（2,22）=8.45，P=0.0007）代谢降低最明显。尾状核轻度代谢低下（-8.4%，与对照组相比，F（2,22）=3.2，P<0.05）。颞叶和额叶未见明显代谢低下。与对照组相比，未发生痴呆的 PD 患者（非 PDD）的初级枕叶皮质（BA 17）的脑代谢降低，仅通过 3D-SSP 分析发现。在研究开始后 2 年对 5 名 PDD 患者进行的随访扫描显示，丘脑（-11.4%）、后扣带回（-9%）、枕叶（-7%）、顶叶（-7%）和额叶（-7%）的脑代谢有明显的间隔内变化，颞叶皮质（-5%）和海马体（-3%）有轻度减少，与研究开始时的扫描相比。
特发性 PD 患者的新发痴呆以视觉联合（BA 18）和后扣带回皮质代谢降低为特征，尾状核也有轻度受累。5 名 PDD 转化者的 2 年随访数据显示，进展为痴呆与涉及中额叶的混合皮质下和皮质变化有关。这些发现为帕金森痴呆的早期代谢特征提供了新的认识。
