Deparment of Radiology, The First Hospital of Lanzhou University, Lanzhou, Gansu, China.
Radiological Clinical Medicine Research Center of Gansu Province, Lanzhou, Gansu, China.
Hum Brain Mapp. 2024 Apr;45(5):e26656. doi: 10.1002/hbm.26656.
Gray matter (GM) atrophy and white matter (WM) lesions may contribute to cognitive decline in patients with delayed neurological sequelae (DNS) after carbon monoxide (CO) poisoning. However, there is currently a lack of evidence supporting this relationship. This study aimed to investigate the volume of GM, cortical thickness, and burden of WM lesions in 33 DNS patients with dementia, 24 DNS patients with mild cognitive impairment, and 51 healthy controls. Various methods, including voxel-based, deformation-based, surface-based, and atlas-based analyses, were used to examine GM structures. Furthermore, we explored the connection between GM volume changes, WM lesions burden, and cognitive decline. Compared to the healthy controls, both patient groups exhibited widespread GM atrophy in the cerebral cortices (for volume and cortical thickness), subcortical nuclei (for volume), and cerebellum (for volume) (p < .05 corrected for false discovery rate [FDR]). The total volume of GM atrophy in 31 subregions, which included the default mode network (DMN), visual network (VN), and cerebellar network (CN) (p < .05, FDR-corrected), independently contributed to the severity of cognitive impairment (p < .05). Additionally, WM lesions impacted cognitive decline through both direct and indirect effects, with the latter mediated by volume reduction in 16 subregions of cognitive networks (p < .05). These preliminary findings suggested that both GM atrophy and WM lesions were involved in cognitive decline in DNS patients following CO poisoning. Moreover, the reduction in the volume of DMN, VN, and posterior CN nodes mediated the WM lesions-induced cognitive decline.
一氧化碳中毒后迟发性神经功能障碍患者的灰质（GM）萎缩和白质（WM）病变可能导致认知能力下降。然而，目前缺乏支持这种关系的证据。本研究旨在调查 33 例痴呆性迟发性神经功能障碍患者、24 例轻度认知障碍性迟发性神经功能障碍患者和 51 名健康对照者的 GM 体积、皮质厚度和 WM 病变负担。采用基于体素、基于变形、基于表面和基于图谱的分析等多种方法来检查 GM 结构。此外，我们还探讨了 GM 体积变化、WM 病变负担与认知能力下降之间的联系。与健康对照组相比，两组患者的大脑皮质（GM 体积和皮质厚度）、皮质下核（GM 体积）和小脑（GM 体积）均存在广泛的 GM 萎缩（p < .05 经 FDR 校正）。包括默认模式网络（DMN）、视觉网络（VN）和小脑网络（CN）在内的 31 个亚区的 GM 总萎缩体积（p < .05，经 FDR 校正）与认知障碍的严重程度独立相关（p < .05）。此外，WM 病变通过直接和间接效应影响认知能力下降，后者由认知网络 16 个亚区的 GM 体积减少介导（p < .05）。这些初步发现表明，GM 萎缩和 WM 病变均与 CO 中毒后迟发性神经功能障碍患者的认知能力下降有关。此外，DMN、VN 和后 CN 节点的体积减少介导了 WM 病变引起的认知能力下降。
