Progressive white-matter demyelination in delayed CO poisoning encephalopathy

Law-Ye, Bruno; Dodet, Pauline; Hermann, Bertrand; Trunet, Stéphanie; Dormont, Didier; Pyatigorskaya, Nadya; Leclercq, Delphine

doi:10.1016/j.neurad.2017.09.008

Cited by 4 publications

(2 citation statements)

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“…Pathologically, the delayed formation of WM lesions is associated with demyelination, which occurs due to the absence of myelin‐related lipids and proteins (Law‐Ye et al, 2018 ; Meyer, 2013 ). The presence of WMH has long been considered indicative of the neuropathology underlying delayed cognitive, motor, psychiatric, and other abnormal symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…Pathologically, the delayed formation of WM lesions is associated with demyelination, which occurs due to the absence of myelinrelated lipids and proteins (Law-Ye et al, 2018;Meyer, 2013) (Chang et al, 2010;Hansen et al, 2014;Tamura et al, 2021). In contrast, even when cognitive impairment improves 1 month after DNS treatment, WM lesions detected on brain MRI persist and may continue beyond 1 year (Hayashi et al, 2022;Inagaki et al, 1997).…”

Section: The Relationship Among Gm Atrophy Wm Lesions Burden and Cogn...mentioning

confidence: 99%

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Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning

Zhang,

Wang,

Wang

et al. 2024

Human Brain Mapping

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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.

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Section: Discussionmentioning

confidence: 99%