Brain structural profile of multiple system atrophy patients with cognitive impairment
Brain structural profile of multiple system atrophy patients with cognitive impairment
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DOI：
10.1007/s00702-016-1636-0
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发表时间：
2017-03-01
影响因子：
3.3
通讯作者：
Biundo, Roberta
中科院分区：
文献类型：
--
作者：
Fiorenzato, Eleonora;Weis, Luca;Biundo, Roberta
目前公认的多系统萎缩(MSA)诊断标准认为痴呆症是一种不支持的特征，尽管在临床实践中报道了认知障碍甚至坦率的痴呆症。简易智力状态检查(MMSE)是一种常用的全球认知量表，在先前的一项研究中，我们建立了MSA特定筛查分界值&27来识别认知障碍。最后，MSA神经成像结果提示认知缺陷患者存在结构变化，尽管解剖变化的程度尚不清楚。我们多中心研究的目的是为了更好地描述与MSA认知损害相关的解剖学变化，并进一步研究皮质和皮质下结构与健康对照组(HC)的差异。我们回顾检查了72名可能的MSA患者[50名认知正常(MSA-NC)和22名认知受损(MSA-CI)]，并使用基于灰质和白质体素的形态测量和全自动皮质下分割将他们与36名HC进行了比较。与HC相比，MSA患者表现为广泛的皮质(双侧额叶、枕颞区和顶区)、皮质下和白质改变。然而，与MSA-NC相比，MSA-CI组仅在左侧背外侧前额叶皮质显示局灶性体积减少。这些结果表明，皮质病理对认知缺陷的贡献微乎其微。我们认为认知功能障碍是由额叶-纹状体局灶性变性引起的，符合“皮质下认知障碍”的概念。
Current consensus diagnostic criteria for multiple system atrophy (MSA) consider dementia a non-supporting feature, although cognitive impairment and even frank dementia are reported in clinical practice. Mini-Mental State Examination (MMSE) is a commonly used global cognitive scale, and in a previous study, we established an MSA-specific screening cut-off score < 27 to identify cognitive impairment. Finally, MSA neuroimaging findings suggest the presence of structural alterations in patients with cognitive deficits, although the extent of the anatomical changes is unclear. The aim of our multicenter study is to better characterize anatomical changes associated with cognitive impairment in MSA and to further investigate cortical and subcortical structural differences versus healthy controls (HC). We examined retrospectively 72 probable MSA patients [50 with normal cognition (MSA-NC) and 22 cognitively impaired (MSA-CI) based on MMSE < 27] and compared them to 36 HC using gray- and white-matter voxel-based morphometry and fully automated subcortical segmentation. Compared to HC, MSA patients showed widespread cortical (bilateral frontal, occipito-temporal, and parietal areas), subcortical, and white-matter alterations. However, MSA-CI showed only focal volume reduction in the left dorsolateral prefrontal cortex compared with MSA-NC. These results suggest only a marginal contribution of cortical pathology to cognitive deficits. We believe that cognitive dysfunction is driven by focal fronto-striatal degeneration in line with the concept of "subcortical cognitive impairment".