Li Zhou1, Xiaoxiao Shan2, Yating Peng3, Guiqian Liu4, Wenbin Guo5, Hong Luo6, Huabing Li7, Dandan Zong8, Ruoyun Ouyang9. 1. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: drzhouli@csu.edu.cn. 2. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; National Clinical Research Center on Mental Disorders, Changsha, Hunan, 410011, China. Electronic address: shanxiaox@csu.edu.cn. 3. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: pengyating2011@126.com. 4. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: 168212143@csu.edu.cn. 5. Department of Psychiatry, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; National Clinical Research Center on Mental Disorders, Changsha, Hunan, 410011, China. Electronic address: guowenbin76@csu.edu.cn. 6. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: luohonghuxi@csu.edu.cn. 7. Department of Radiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. Electronic address: huabingli3350@csu.edu.cn. 8. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: zongdandan0402@csu.edu.cn. 9. Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China; Research Unit of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China; Diagnosis and Treatment Center of Respiratory Disease, Central South University, Changsha, Hunan, 410011, China. Electronic address: ouyangruoyun@csu.edu.cn.
Abstract
BACKGROUND: Neurocognitive dysfunction and abnormal regional homogeneity (ReHo) have been reported in patients with obstructive sleep apnea (OSA). However, little is known about whether brain functional alteration could be used to differentiate from healthy controls (HCs) and its correlation with neurocognitive impairment. METHODS: Thirty-three treatment-naive patients with moderate-to-severe OSA and 22 HCs with matched age, sex and education underwent the evaluation of Epworth sleepiness scale, neurocognitive function, full night polysomnography and resting-state functional magnetic resonance imaging scan. ReHo, support vector machine, and correlation with neurocognitive function were administrated to analyze the data. RESULTS: Compared with HCs, patients with OSA showed decreased ReHo in the bilateral superior frontal gyrus (FG), bilateral superior medial prefrontal cortex (PFC)/right supplementary motor area (SMA), left middle FG, and right precentral/postcentral gyrus. Negative correlations were observed between the ReHo values in the left superior FG/middle FG and apnea hypopnea index, oxygen desaturation index in the OSA group. The scores of Stroop word test, Stroop color-word test, symbol coding test were all negatively correlated with the ReHo values in the right precentral gyrus/postcentral gyrus in patients. Scores of the animal naming fluency test were positively correlated with the ReHo values in the left superior FG/middle FG in patients. Moreover, support vector machine analysis showed the ReHo values in the left superior FG/middle FG or bilateral superior medial PFC/right SMA both could discriminate patients from HCs with good accuracies, sensitivities, and specificities (85.45%, 87.88%, 81.82% and 81.82%, 84.85%, 77.27%, respectively). CONCLUSION: Dysfunction in the frontal lobe is a potentially pivotal neuro-pathophysiological mechanism of neurocognitive impairment in patients with moderate-to-severe OSA. And significantly lower ReHo values in the left superior FG/middle FG and/or superior medial PFC/SMA are promising imaging biomarkers to discriminate moderate-to-severe patients with OSA from HCs.
BACKGROUND:Neurocognitive dysfunction and abnormal regional homogeneity (ReHo) have been reported in patients with obstructive sleep apnea (OSA). However, little is known about whether brain functional alteration could be used to differentiate from healthy controls (HCs) and its correlation with neurocognitive impairment. METHODS: Thirty-three treatment-naive patients with moderate-to-severe OSA and 22 HCs with matched age, sex and education underwent the evaluation of Epworth sleepiness scale, neurocognitive function, full night polysomnography and resting-state functional magnetic resonance imaging scan. ReHo, support vector machine, and correlation with neurocognitive function were administrated to analyze the data. RESULTS: Compared with HCs, patients with OSA showed decreased ReHo in the bilateral superior frontal gyrus (FG), bilateral superior medial prefrontal cortex (PFC)/right supplementary motor area (SMA), left middle FG, and right precentral/postcentral gyrus. Negative correlations were observed between the ReHo values in the left superior FG/middle FG and apnea hypopnea index, oxygen desaturation index in the OSA group. The scores of Stroop word test, Stroop color-word test, symbol coding test were all negatively correlated with the ReHo values in the right precentral gyrus/postcentral gyrus in patients. Scores of the animal naming fluency test were positively correlated with the ReHo values in the left superior FG/middle FG in patients. Moreover, support vector machine analysis showed the ReHo values in the left superior FG/middle FG or bilateral superior medial PFC/right SMA both could discriminate patients from HCs with good accuracies, sensitivities, and specificities (85.45%, 87.88%, 81.82% and 81.82%, 84.85%, 77.27%, respectively). CONCLUSION: Dysfunction in the frontal lobe is a potentially pivotal neuro-pathophysiological mechanism of neurocognitive impairment in patients with moderate-to-severe OSA. And significantly lower ReHo values in the left superior FG/middle FG and/or superior medial PFC/SMA are promising imaging biomarkers to discriminate moderate-to-severe patients with OSA from HCs.