Brain functional activity and connectivity alterations induced by acute carbon monoxide poisoning contribute to delayed neuropsychiatric sequelae

The brain functional activity and connectivity alterations induced by acute carbon monoxide (CO) poisoning may contribute to delayed neurological sequelae (DNS) and be associate with the poisoning severities, although comprehensive evidence remains limited. Seventy-four subjects were prospectively recruited for this study, comprising eighteen DNS patients, twenty-six non-DNS patients, and thirty healthy controls. The study employed analysis methods such as the amplitude of low-frequency fluctuation, regional homogeneity, weighted degree centrality, secondary seed-based functional connectivity (FC), and Granger causality analysis to assess functional activity and connectivity. Partial correlation analyses between extracted abnormal functional indices and clinical variables including duration of CO exposure and Glasgow Coma Scale scores were further explored. The results showed that DNS patients exhibited altered functional activity in specific nodes of the visual network (VN), sensorimotor network (SMN), and executive control network (ECN) (Gaussian random field [GRF]-corrected, P < 0.05). Additionally, altered FC values were detected in the nodes of the VN, default mode network (DMN), ECN, SMN, and the cerebello-cortical motor loop nodes (GRF-corrected, P < 0.05). VN hyperactivity exerted inhibitory effects on the DMN and SMN, as well as self-inhibition within DMN nodes. Conversely, DMN nodes showed hypoactivity and received excitatory influences from the anterior cerebellar and ECN nodes. Connectivity changes of above networks and loop nodes were associated with the clinical severities (Bonferroni-corrected, P < 0.05). These findings highlight significant changes in neural functional activity and connectivity across cognitive and motor-related network nodes, potentially contributing to DNS development and associating with the poisoning severities.