Influence of Propofol-Induced Sedation on White Matter Functional Connectivity
Jiayi Zhang1, Minyu Jian2, Leqing Zhou1
1From the School of Artificial Intelligence, Beijing University of Posts and Telecommunications, Beijing, China.
Background:
Propofol is a commonly used anesthetic, and its impact on brain function has been a significant focus of neuroscience research. However, previous studies have primarily focused on the effects of propofol on gray matter function. White matter in the brain is a pathway for transmitting information between different brain regions. Recently, blood oxygen level-dependent signals in white matter have been shown to have physiological significance. However, the effects of propofol on white matter function remain unclear. The purpose of this study is to investigate changes in white matter functional connectivity during propofol-induced sedation.
Methods:
Resting-state functional magnetic resonance imaging was performed on 21 healthy participants in four states: awake, mild propofol-induced sedation, deep propofol-induced sedation, and postsedation recovery. White matter functional connectivity, including white to gray matter functional connectivity and white to white matter functional connectivity, was compared between different states. The white matter tracts primarily affected by propofol were identified by calculating white matter functional connectivity strength from white to gray matter functional connectivity and performing a Friedman test across four states. Additionally, considering that white matter promotes gray matter communication, white matter-mediated functional networks were constructed through white to gray matter functional connectivity. The global efficiency of white matter-mediated functional networks across different states was studied.
Results:
The white to gray matter functional connectivity and white to white matter functional connectivity significantly decreased during deep sedation compared to the awake state (P < .05). Several fiber tracts, including the posterior limb of the internal capsule, the cingulum near the cingulate gyrus, the genu of corpus callosum, and the retrolenticular part of the internal capsule, showed significant differences in white matter functional connectivity strength across the four states (P < .01). The global efficiency of the whole brain network, as well as the visual, somatomotor, attention, frontoparietal, limbic, and default mode networks, decreased during deep sedation and returned to the awake level after recovery (P < .05).
Conclusions:
Propofol disrupts white matter functional connectivity, with deep sedation inducing widespread functional connectivity reductions, particularly in key tracts and networks. The disruption of white matter functional connectivity may reflect a breakdown in large-scale brain integration and could serve as a biomarker for deep propofol-induced sedation, although not necessarily its mechanistic driver.
