DocumentCode
3685177
Title
Spontaneous neuronal activity in insula predicts symptom severity of unmedicated obsessive compulsive disorder adults
Author
Y. Zhu;Q. Fan;Z. Zhang;H. Zhang;S. Tong;Y. Li
Author_Institution
School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, 200030, China
fYear
2015
Firstpage
5445
Lastpage
5448
Abstract
Emerging evidence has suggested that the pathophysiology of obsessive compulsive disorder (OCD) might involve widely distributed large-scale brain systems. The dysfunction within salience network, which is comprised of dorsal anterior cingulated cortex (dACC) and bilateral insular areas, has been proposed to contribute to OCD onset. The mechanism underlying salience network abnormality remains unclear and it is worthwhile to investigate its clinical relevance using functional neuroimaging approaches. In this study, we performed the spontaneous brain activity measurement using resting-state functional magnetic resonance imaging (fMRI) on unmedicated OCD patients (n=23). Specifically, the amplitude of low frequency (0.01-0.08 Hz) fluctuations (ALFF) was calculated for regions in salience network. The voxel-based Pearson´s correlative analysis was conducted to explore the relationship beween ALFF measures and symptom severity for OCD patients. The results showed that the spontaneous neuronal activity in insula was significantly correlated to OCD clinical symptoms, especially compulsive behaviors. Our findings consolidated that the salience network played an important role in the pathogenesis of OCD and the intensity of intrinsic brain activity in insula provided a predictive biomarker for OCD symptom severity.
Keywords
"Magnetic resonance imaging","Yttrium","Brain","Correlation","Head","Magnetic heads","Neuroimaging"
Publisher
ieee
Conference_Titel
Engineering in Medicine and Biology Society (EMBC), 2015 37th Annual International Conference of the IEEE
ISSN
1094-687X
Electronic_ISBN
1558-4615
Type
conf
DOI
10.1109/EMBC.2015.7319623
Filename
7319623
Link To Document