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Aberrant interhemispheric resting state functional connectivity and corpus callosum microstructure in acute carbon
Mingyue Ma1, Yu Shang2, Xiaoying Lin3
1Department of Medical Imaging, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; Department of Radiology, the Affiliated Xi'an Central Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
None:
Acute carbon monoxide poisoning (ACOP) is a significant contributor to acute poisoning incidents worldwide, with numerous patients suffering from cognitive impairment. Growing evidence indicates that patients with ACOP exhibit both disrupted functional connectivity and corpus callosum (CC) degeneration. Nevertheless, how interhemispheric connectivity is altered in ACOP and how such alterations relate to cognitive deficits remain largely unexplored. In this study, multimodal magnetic resonance imaging was performed on 30 patients with ACOP and 28 healthy controls (HC), and their cognitive functions were evaluated. Group differences in the voxel-mirrored homotopic connectivity (VMHC) index and CC white matter microstructure were analyzed. Furthermore, mediation analysis was conducted to elucidate the interrelationships among CC integrity, interhemispheric connectivity, and cognitive impairment. Compared to HC, patients with ACOP exhibited reduced VMHC values in the middle frontal gyrus, inferior parietal lobule, precentral gyrus, and temporal regions, along with decreased fractional anisotropy values in the subregions of the CC, including the genu, body, and splenium. Partial correlation analyses showed that VMHC in the inferior parietal lobule positively correlated with Glasgow Coma Scale scores. In addition, VMHC in both the inferior parietal lobule and the middle temporal gyrus positively correlated with Montreal Cognitive Assessment-Basic scores. Mediation analysis indicated that changes in interhemispheric connectivity played a crucial role in mediating the effect of CC integrity on cognitive impairment. Together, these findings may offer novel insights into the neurobiological mechanisms underlying ACOP.
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