Neural correlates of cognitive impairment in posterior cortical atrophy
Neural correlates of cognitive impairment in posterior cortical atrophy
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DOI：
10.1093/brain/awr055
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发表时间：
2011-05-01
期刊：
影响因子：
14.5
通讯作者：
Sarazin, Marie
中科院分区：
文献类型：
--
作者：
Kas, Aurelie;de Souza, Leonardo Cruz;Sarazin, Marie
随着针对阿尔茨海默病的病理生理过程的疾病修饰药物的前景，现在至关重要的是增加对阿尔茨海默病的非典型局灶性表现的理解，如后皮质萎缩。本研究旨在（i）使用感兴趣区域和基于体素的方法表征后皮质萎缩的脑灌注特征;（ii）研究疾病持续时间对临床和成像特征的影响;（iii）探索脑灌注与认知缺陷之间的相关性。39例后皮质萎缩的患者接受了一系列神经心理学测试，主要针对视觉空间功能，以及Tc-99 m-乙基半胱氨酸二聚体脑灌注造影。影像学分析包括与24名阿尔茨海默病患者（年龄、病程和简易精神状态检查相匹配）和24名健康对照组的比较。后皮质萎缩患者的单光子发射计算机断层扫描特征为枕叶、顶叶、后颞叶皮质和对应于额叶视野的较小皮质区（Brodmann 6/8区）广泛和严重灌注不足。与阿尔茨海默病患者相比，后皮质萎缩组表现出更严重的枕顶低灌注和更高的灌注额，前扣带回和近中颞区。当考虑到疾病的持续时间，功能变化开始并保持集中在后叶，即使在晚期。后皮质萎缩的脑灌注和神经心理学评分的相关性分析突出了左下顶叶损伤在计算能力丧失、Gerstmann综合征、左右模糊和肢体失用中的突出作用，而双侧枕顶背侧区的损伤似乎与Balint综合征有关。我们的研究结果提供了新的见解，根据疾病持续时间的功能变化的自然史，并强调顶叶和枕叶皮质的作用，在认知综合征的特点后皮质萎缩。
With the prospect of disease-modifying drugs that will target the physiopathological process of Alzheimer's disease, it is now crucial to increase the understanding of the atypical focal presentations of Alzheimer's disease, such as posterior cortical atrophy. This study aimed to (i) characterize the brain perfusion profile in posterior cortical atrophy using regions of interest and a voxel-based approach; (ii) study the influence of the disease duration on the clinical and imaging profiles; and (iii) explore the correlations between brain perfusion and cognitive deficits. Thirty-nine patients with posterior cortical atrophy underwent a specific battery of neuropsychological tests, mainly targeting visuospatial functions, and a brain perfusion scintigraphy with Tc-99m-ethyl cysteinate dimer. The imaging analysis included a comparison with a group of 24 patients with Alzheimer's disease, matched for age, disease duration and Mini-Mental State Examination, and 24 healthy controls. The single-photon emission computed tomography profile in patients with posterior cortical atrophy was characterized by extensive and severe hypoperfusion in the occipital, parietal, posterior temporal cortices and in a smaller cortical area corresponding to the frontal eye fields (Brodmann areas 6/8). Compared with patients with Alzheimer's disease, the group with posterior cortical atrophy showed more severe occipitoparietal hypoperfusion and higher perfusion in the frontal, anterior cingulate and mesiotemporal regions. When considering the disease duration, the functional changes began and remained centred on the posterior lobes, even in the late stage. Correlation analyses of brain perfusion and neuropsychological scores in posterior cortical atrophy highlighted the prominent role of left inferior parietal damage in acalculia, Gerstmann's syndrome, left-right indistinction and limb apraxia, whereas damage to the bilateral dorsal occipitoparietal regions appeared to be involved in Balint's syndrome. Our findings provide new insight into the natural history of functional changes according to disease duration and highlight the role of parietal and occipital cortices in the cognitive syndromes that characterize the posterior cortical atrophy.