| Objective: The purpose of this study is to analyze the potential relationship between the changes of neuronal spontaneous activity,gray structure and functional connectivity and cognitive and emotional function in patients with obstructive sleep apnea(OSA),from resting state brain function and brain structure,using magnetic resonance imaging technology,and provide imaging evidence for further elucidating the neuropathophysiological mechanism of brain damage in OSA patients.Methods: In total,66 treatment-na?ve,newly diagnosed patients with OSA(OSA group),and 88 well-matched healthy controls(control group)were continuously collected and underwent brain MRI scan and neuropsychological scale assessment.DPABI_V6.1 and SPM12(cat12 toolbox)software were used to compare the regional homogeneity(Re Ho),fractional amplitude of low frequency fluctuation(f ALFF),gray matter volume(GMV),and Surface morphology of gray matter(including cortical thickness,sulcus depth,gyrification index and fractal dimension)between groups by two-sample t test.Define the seed regions after analyzing statistically significant differences between the two groups,and then calculate the functional connectivity between the seed regions and each voxel in the whole brain.The two-sample t test was performed to obtain the statistically different brain regions.Demographic and clinical characteristics in OSA and control groups were compared with SPSS 25.0 soft.Linear correlation and multiple linear stepwise regression analysis were used to further evaluate the correlations between the parameter values of the different brain regions and clinical characteristics(including body mass index,disease duration,sleep monitoring indicators and neuropsychological scale scores)in OSA group.Results: Compared with control group,the OSA group showed decreased f ALFF values in left middle occipital gyrus and right cerebellum CrusⅡ area,and increased f ALFF values in the right hippocampus,right parahippocampal gyrus,right orbital superior frontal gyrus and left thalamus.The Re Ho values increased in the right parahippocampal gyrus(gaussian random field multiple comparison correction,voxel-level P<0.001,cluster-level P<0.05).The OSA group showed reduced GMV in the right fusiform gyrus,superior occipital gyrus,middle cingulate cortex,left superior temporal gyrus and left lingual gyrus(voxel-level P <0.001,voxel number >100).The thickness thinner existed in right superior frontal gyrus and right middle cingulate cortex,and sulcus depth decrease existed in right inferior temporal gyrus and right fusiform gyrus(P<0.05,false discovery rate corrected for multiple comparisons).The OSA group showed enhanced functional connectivity between right fusiform gyrus and bilateral putamen and left supplementary motor area(gaussian random field multiple comparison correction,voxel-level P<0.001,cluster-level P<0.05).In addition,compared with control group,OSA group had higher body mass index,depression scale scores,anxiety scale scores and sleep related scales scores,and lower cognitive function scale scores.The abnormal brain regions of spontaneous activity,gray matter structure and functional connectivity were correlated with clinical characteristics in OSA group.Conclusions:(1)This study found that OSA patients have a high body mass index,high risk of depression,anxiety,and cognitive impairment.(2)Atrophy of gray matter in the superior frontal gyrus,superior occipital gyrus,temporal lobe,fusiform gyrus,middle cingulate and lingual gyrus was found in OSA patients.Abnormal spontaneous activity of neurons in the middle occipital gyrus,cerebellum CrusⅡ,hippocampus,parahippocampal gyrus,supraorbital frontal gyrus and thalamus were found in OSA patients using resting-state functional magnetic resonance imaging.It may be an important neuroimaging basis for OSA brain damage.(3)The functional connectivity between the fusiform gyrus and supplementary motor area is enhanced in OSA patients,which is positively correlated with the total Mo CA score and memory score,providing new insights into the neuropathophysiological mechanism of cognitive memory impairment in OSA patients. |