Clinical Neurophysiology, Dept. of Neurosciences, Ophthalmology and Genetics, University of Genoa, Genoa, Italy.
J Neurol Sci. 2011 Nov 15;310(1-2):31-5. doi: 10.1016/j.jns.2011.06.053. Epub 2011 Jul 16.
A subtle cognitive impairment can be detected early in the course of Parkinson's disease (PD). Executive, memory and visuospatial functions are specifically affected, but the underlying pathophysiological basis is not well elucidated yet and may be heterogeneous. The recent identification of a PD-related cognitive metabolic pattern (PDCP), including hypometabolism in associative frontal, parietal and posterior limbic structures, has integrated the classical notion of a striato-frontal syndrome at the basis of cognitive dys-function. Recent evidence suggests that whilst executive dys-function is seen in virtually all PD patients, visuospatial and memory impairment may share a higher risk for the subsequent development of dementia. By means of perfusion SPECT and [18F]FDG-PET, cortical dys-function may be highlighted since the early stages, it is more evident in PD patients with Mild Cognitive Impairment (MCI), and reaches the maximum in PD dementia (PDD). Posterior temporo-parieto-occipital dys-function in associative and limbic cortex, closely resembling that found in Alzheimer's disease patients, is found in PDD, with a more severe occipital hypometabolism and a relatively milder hypometabolism in medial temporal lobe structures. Furthermore, deficit of acetylcholinesterase (AchE) can be found by means of [11C]MP4A-PET already in early stage of PD, especially in posterior regions, then becoming more severe in PDD and in dementia with Lewy bodies (DLB). Administration of AchE inhibitors to PDD patients increased brain metabolism in bilateral frontal and left parietal regions, and left posterior cingulate. Finally, the recent availability of radiopharmaceuticals able to disclose amyloid brain deposition has allowed to demonstrate amyloid load in a part of patients with PDD, possibly due to diffuse rather than neuritic plaques. Brain PET and SPECT have strongly contributed to the understanding of the pathophysiology of cognitive impairment in PD and may serve as probes to monitor the effects of therapeutic interventions.
帕金森病（PD）早期即可检测到轻微的认知障碍。执行、记忆和视空间功能受到特别影响，但潜在的病理生理基础尚未得到很好的阐明，可能具有异质性。最近发现的与 PD 相关的认知代谢模式（PDCP），包括与关联的额、顶和后边缘结构的代谢降低，整合了认知功能障碍基础上的纹状体-额综合征的经典概念。最近的证据表明，虽然几乎所有 PD 患者都存在执行功能障碍，但视空间和记忆障碍可能具有更高的风险发展为痴呆。通过灌注 SPECT 和 [18F]FDG-PET，可以突出皮质功能障碍，因为它在早期阶段更为明显，在轻度认知障碍（MCI）的 PD 患者中更为明显，在 PD 痴呆（PDD）中达到最大值。在关联和边缘皮质的后颞顶枕叶功能障碍，与阿尔茨海默病患者相似，在 PDD 中发现，枕叶代谢降低更严重，内侧颞叶结构代谢降低更轻。此外，通过 [11C]MP4A-PET 可以发现乙酰胆碱酯酶（AchE）的缺失，特别是在 PD 的早期阶段，尤其是在后区，然后在 PDD 和路易体痴呆（DLB）中变得更严重。给予 AchE 抑制剂可增加 PDD 患者双侧额和左顶叶以及左后扣带回的脑代谢。最后，最近可获得的能够显示淀粉样蛋白脑沉积的放射性药物已允许在一部分 PDD 患者中显示淀粉样蛋白负荷，可能是由于弥漫性而非神经纤维状斑块。脑 PET 和 SPECT 极大地促进了对 PD 认知障碍的病理生理学的理解，并可能作为监测治疗干预效果的探针。
