Abnormal Brain Functional Network Dynamics in Acute CO Poisoning

Abstract

Aims: Carbon monoxide poisoning is a common condition that can cause severe neurological sequelae. Previous studies have revealed that functional connectivity in carbon monoxide poisoning is abnormal under the assumption that it is resting during scanning and have focused on studying delayed encephalopathy in carbon monoxide poisoning. However, studies of functional connectivity dynamics in the acute phase of carbon monoxide poisoning may provide a more insightful perspective for understanding the neural mechanisms underlying carbon monoxide poisoning. To our knowledge, this is the first study that explores abnormal brain network dynamics in the acute phase of carbon monoxide poisoning.Methods: Combining the sliding window method and k-means algorithm, we identified four recurrent dynamic functional cognitive impairment states from resting-state functional magnetic resonance imaging data from 29 patients in the acute phase of carbon monoxide poisoning and 29 healthy controls. We calculated between-group differences in the temporal properties and intensity of dFC states, and we also performed subgroup analyses to separately explore the brain network dynamics characteristics of adult vs. child carbon monoxide poisoning groups. Finally, these differences were correlated with patients’ cognitive performance in the acute phase of carbon monoxide poisoning and coma duration.Results: We identified four morphological patterns of brain functional network connectivity. During the acute phase of carbon monoxide poisoning, patients spent more time in State 2, which is characterized by positive correlation between SMN and CEN, and negative correlation between DMN and SMN. In addition, the fractional window and mean dwell time of State 2 were positively correlated with coma duration. The subgroup analysis results demonstrated that the acute phase of childhood carbon monoxide poisoning had greater dFNC time variability than adult carbon monoxide poisoning.Conclusion: Our findings reveal that patients in the acute phase of carbon monoxide poisoning exhibit dynamic functional abnormalities. Furthermore, children have greater dFNC instability following carbon monoxide poisoning than adults. This advances our understanding of the pathophysiological mechanisms underlying acute carbon monoxide poisoning.

A Graph Theory Study of Resting‐State Functional MRI Connectivity in Children With Carbon Monoxide Poisoning

“…6,35,36 In addition, the group of CO poisoned children showed a neural circuit with enhanced connection strength, principally concentrated in the auditory and visual cortices. Consistent with our previous study, 8 there was either within-network or between-network functional connectivity augmentation in the visual network and auditory network after CO poisoning, which was attributed to the compensatory mechanism. These findings demonstrate that CO poisoning leads to changes in the topological properties of functional areas in the brain and abnormalities in neural circuits, expanding our understanding of the pathophysiological mechanisms of CO poisoning.…”

“…Most of the current studies on CO poisoning are concentrated on cerebral structural changes and [3][4][5][6][7] little is devoted to the early cerebral function. 8,9 The lack of detailed studies on the changes of brain functional networks after CO poisoning, especially in young patients with rapidly developing brain functions, limits our comprehensive understanding of the disease caused by CO poisoning.…”

A patient with toxic encephalopathy associated with acute carbon monoxide poisoning–A clinical case

“…DEACMP patients suffer a series of neurological and psychiatric disorders, including cognitive dysfunction, motor impairment, extrapyramidal systems dysfunction, even consciousness disturbance after a brief lucid period, cortical blindness, depression. DEACMP may be caused by secondary brain tissue damage, due to CO-mediated brain tissue hypoxia, oxygen-based free radicals, and membrane peroxidation, instead of due to direct hypoxia-induced damage [16][17][18][19].…”