Based on resting-state functional MRI (fMRI), we preliminarily explored brain alterations in asymptomatic patients with vulnerable carotid plaques, but carotid stenosis was < 50%.
A total of 58 asymptomatic patients with vulnerable carotid plaques (stenosis <50%) and 38 healthy controls were recruited. Between-group differences in regional homogeneity (ReHo), degree centrality (DC), and functional connectivity (FC) were analyzed. Correlation analysis was performed between the ReHo or DC values in altered brain regions as well as voxel-wise abnormal FC and scores on neuropsychiatric scales, serum interleukin-6 (IL-6), and C-reactive protein (CRP).
Both ReHo and DC values on the left superior occipital gyrus (SOG.L) of the asymptomatic vulnerable carotid plaque group reduced, regardless of plaque location (left, right, or bilateral). Functional connections weakened between the SOG.L and right lingual gyrus (LING.R)/right inferior occipital gyrus (IOG.R), right middle frontal gyrus (MFG.R)/orbital part of superior frontal gyrus (ORBsup.R)/orbital part of middle frontal gyrus (ORBmid.R), left precentral gyrus (PreCG.L)/postcentral gyrus (PoCG.L), left supplementary motor area (SMA.L), right paracentral lobule (PCL.R), left precuneus (PCUN.L), and right postcentral gyrus (PoCG.R)/PCL.R. In ReHo-altered brain regions, ReHo values were positively correlated with Hamilton Rating Scale for Depression (HAMD) scores, and the setting region of abnormal ReHo as seed points, voxel-wise FC between the SOG.L and PreCG.L was negatively correlated with CRP.
Cerebral alterations of neuronal synchronization, activity, and connectivity properties in the asymptomatic vulnerable carotid plaque group were independent of the laterality of vulnerable carotid plaques. Significant relation between ReHo values on the SOG.L and HAMD indicated that even when there were neither clinical symptoms nor lesions on routine MRI, brain function might have changed already at an early stage of carotid atherosclerosis. Inflammation might play a role in linking vulnerable carotid plaques and changes of resting-state functional connectivity.