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Original Research

Disrupted resting-state spontaneous neural activity in stable COPD

, , , , , & show all
Pages 499-508 | Published online: 27 Feb 2019
 

Abstract

Introduction and aim

Abnormal brain structure and function in COPD has been reported on MRI. However, the deficit in local synchronization of spontaneous activity in patients with stable COPD remains unknown. The main aim of the present study was to explore spontaneous brain activity in patients with COPD compared with normal controls using the regional homogeneity (ReHo) method based on resting-state functional MRI.

Methods

Nineteen patients with stable COPD and 20 well-matched (including age, sex, and number of years of education) normal controls who were recruited for the present study underwent resting-state functional MRI examinations and a series of neuropsychological and clinical assessments. The ReHo method was used to assess the strength of local brain signal synchrony. The mean ReHo values in brain areas with abnormal ReHo were evaluated with a receiver operating characteristic curve. The relationships between the brain regions with altered ReHo values and the clinical and neuropsychological parameters in COPD patients were assessed using Pearson’s correlation.

Results

Patients with COPD showed significantly lower ReHo values in the left occipital lobe and the right lingual, bilateral precuneus, and right precentral gyrus. The result of receiver operating characteristic curve analysis showed that the altered average ReHo values have high efficacy for distinguishing function. The mean lower ReHo values in the precuneus gyrus showed a significant positive correlation with FEV1%, FEV1/FVC, and orientation function but a significant negative correlation with arterial partial pressure of carbon dioxide.

Conclusion

The COPD patients demonstrated abnormal synchrony of regional spontaneous activity, and the regions with abnormal activity were all correlated with visual processing pathways, which might provide us with a new perspective to further understand the underlying pathophysiology of cognitive impairment in patients with COPD.

Acknowledgments

This study was supported by the Natural Science Foundation of China (grant numbers 81860307 and 81560285), the Natural Science Foundation Project of Jiangxi, China (grant numbers 20171BAB205070 and 20181ACB20023), Education Department Project of Jiangxi Province, China (grant numbers 700544006), Department of Health Project and Jiangxi Province, China (grant number 20181039), and the Graduate Innovation Foundation of Jiangxi, China (grant number YC2018-S099).

Disclosure

The authors report no conflicts of interest in this work.