Structural, Microstructural, and Metabolic Alterations in Primary Progressive Aphasia Variants
Structural, Microstructural, and Metabolic Alterations in Primary Progressive Aphasia Variants
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DOI：
10.3389/fneur.2018.00766
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发表时间：
2018-09-18
影响因子：
3.4
通讯作者：
Teichmann, Marc
中科院分区：
文献类型：
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作者：
Routier, Alexandre;Habert, Marie-Odile;Teichmann, Marc
神经影像学研究已经描述了原发性进行性失语症（PPA）变体（语义、逻辑缺失、不流利/语法缺失）的大脑改变。然而，很少有研究结合T1，FDG-PET和弥散MRI技术来研究三种PPA主要变体的萎缩，低代谢和束改变。因此，我们探索了一个大型的早期队列的语义，logopenic和nonfluent/agrammatic变体（N = 86）和23匹配的健康对照与解剖MRI（皮质厚度），FDG PET（代谢）和扩散MRI（白色物质束分析），旨在确定皮质和皮质下的大脑改变，并面对这些改变的成像方式和失语症的变种。在语义变异中，前颞叶皮质变薄和代谢减退，左半球占优势，向后颞区延伸，并影响投射到前颞叶的神经束（下纵束、钩束）和投射到后颞叶皮质或在其附近运行的神经束（上级纵束、下额枕束）。在logopenic变量的代谢变化更广泛的萎缩，主要影响左颞顶叶交界处，并延伸到更多的前颞叶皮质。考虑到左侧上级和下级纵束以及左侧额枕下束的改变，代谢和束数据是一致的。在非流畅/语法缺失的变体中，皮质变薄和代谢低下位于左额叶皮质，但布洛卡区仅受到代谢指标的影响。与布罗卡区连接的左侧钩束损伤反映了代谢和束改变的一致性。我们的研究结果提供了一个全面的统计学上强大的图片，在早期变异的原发性进行性失语症，这对诊断，分类和未来的治疗策略的影响大脑的变化。他们表明，在逻辑和语义的变化模式的脑损伤显示不可忽略的重叠在颞区，而它们是基本上不同的nonfluent/agrammatic变量（额叶）。这些结果还表明，额叶网络（组合语法/语音）和时间网络（词汇/语义表示）构成不同的解剖功能实体与失语症变体的退化过程的差异脆弱性。最后，识别特定的损伤模式可以通过指示适当的目标进入受损的语言系统，为经颅刺激方法开辟一条途径。
Neuroimaging studies have described the brain alterations in primary progressive aphasia (PPA) variants (semantic, logopenic, nonfluent/agrammatic). However, few studies combined T1, FDG-PET, and diffusion MRI techniques to study atrophy, hypometabolism, and tract alterations across the three PPA main variants. We therefore explored a large early-stage cohort of semantic, logopenic and nonfluent/agrammatic variants (N = 86) and of 23 matched healthy controls with anatomical MRI (cortical thickness), FDG PET (metabolism) and diffusion MRI (white matter tracts analyses), aiming at identifying cortical and sub-cortical brain alterations, and confronting these alterations across imaging modalities and aphasia variants. In the semantic variant, there was cortical thinning and hypometabolism in anterior temporal cortices, with left-hemisphere predominance, extending toward posterior temporal regions, and affecting tracts projecting to the anterior temporal lobes (inferior longitudinal fasciculus, uncinate fasciculus) and tracts projecting to or running nearby posterior temporal cortices: (superior longitudinal fasciculus, inferior frontal-occipital fasciculus). In the logopenic variant metabolic alterations were more extensive than atrophy affecting mainly the left temporal-parietal junction and extending toward more anterior temporal cortices. Metabolic and tract data were coherent given the alterations of the left superior and inferior longitudinal fasciculus and the left inferior frontal-occipital fasciculus. In the nonfluent/agrammatic variant cortical thinning and hypometabolism were located in the left frontal cortex but Broca's area was only affected on metabolic measures. Metabolic and tract alterations were coherent as reflected by damage to the left uncinate fasciculus connecting with Broca's area. Our findings provide a full-blown statistically robust picture of brain alterations in early-stage variants of primary progressive aphasia which has implications for diagnosis, classification and future therapeutic strategies. They demonstrate that in logopenic and semantic variants patterns of brain damage display a non-negligible overlap in temporal regions whereas they are substantially distinct in the nonfluent/agrammatic variant (frontal regions). These results also indicate that frontal networks (combinatorial syntax/phonology) and temporal networks (lexical/semantic representations) constitute distinct anatomo-functional entities with differential vulnerability to degenerative processes in aphasia variants. Finally, the identification of the specific damage patterns could open an avenue for trans-cranial stimulation approaches by indicating the appropriate target-entry into the damaged language system.