Altered functional connectivity within default mode network after rupture of anterior communicating artery aneurysm

BACKGROUND: Rupture of anterior communicating artery (ACoA) aneurysm often leads to cognitive impairment, especially memory complaints. The medial superior frontal gyrus (SFGmed), a node of the default mode network (DMN), has been extensively revealed to participate in various cognitive processes. However, the functional connectivity (FC) characteristics of SFGmed and its relationship with cognitive performance remain unknown after the rupture of the ACoA aneurysm. METHODS: Resting-state functional MRI (fMRI) and cognitive assessment were acquired in 27 eligible patients and 20 controls. Seed-based FC between unilateral SFGmed and the rest of the brain was calculated separately, and then compared their intensity differences between the two groups. Furthermore, we analyzed the correlation between abnormal FC and cognitive function in patients with ruptured ACoA aneurysm. RESULTS: Cognitive impairment was confirmed in 51.9% of the patients. Compared with the controls, patients suffering from ruptured ACoA aneurysm exhibited a similar FC decline between each side of SFGmed and predominant nodes within DMN, including the precuneus, angular gyrus, cingulate cortex, left hippocampus, left amygdala, left temporal pole (TPO), and left medial orbitofrontal cortex (mOFC). Besides, significantly decreased FC of left SFGmed and left insula, right middle temporal gyrus (MTG), as well as right mOFC, were also found. In addition, only enhanced insular connectivity with right SFGmed was determined, whereas increased FC of the left SFGmed was not observed. Correlation analyses showed that lower total cognitive performance or stronger subjective memory complaints were related to reduced connectivity in the SFGmed and several cortical regions such as the angular gyrus and middle cingulate cortex (MCC). CONCLUSION: Our results suggest that patients with ruptured ACoA aneurysm exist long-term cognitive impairment and intrinsic hypoconnectivity of cognition-related brain regions within DMN. Deactivation of DMN may be a potential neural mechanism leading to cognitive deficits in these patients.