Brain functional and structural alteration following acute carbon monoxide poisoning contribute to delayed neurological sequelae.

PURPOSE: To investigate whether altered functional activity, functional connectivity (FC), and structural connectivity (SC) following acute carbon monoxide (CO) poisoning contribute to delayed neurological sequelae (DNS) occurrence.

METHODS

Binary degree centrality (DC) and seed-based FC were investigated in 18 patients with DNS, 26 patients without DNS, and 30 healthy controls. Duration of CO exposure and coma severity indices-related fibers was detected by connectometry analysis and the identified fiber tracts were tracked and their SC alteration was quantify by fractional anisotropy (FA).

RESULTS

Acute CO exposure induced DC change in the prefrontal cortex (PFC), visual cortex, primary sensory cortex, and anterior cerebellum, and FC alteration between the right fusiform gyrus (seed) and bilateral PFC and left inferior occipital gyrus (Gaussian random field corrected, P < 0.05). Poisoning severity indices-related WM fibers consisted of corpus callosum and some association and projection fibers (false discovery rate corrected, P < 0.05). Only altered DC in the right fusiform gyrus and right postcentral gyrus and reduced FC of the PFC could identify DNS occurrence (P < 0.05).

CONCLUSIONS

The functional abnormalities in the visual- and sensory- cortex and PFC subsequent to acute CO poisoning represent one of the potential neural mechanisms underlying the occurrence of DNS.