Abnormal regional homogeneity and functional connectivity in adjustment disorder of new recruits: a resting-state fMRI study

Purpose To explore the regional spontaneous neural activity and functional connectivity alterations of adjustment disorder (AD) in new recruits with in vivo resting-state functional MR (rs-fMRI). Materials and methods Resting-state fMRI was performed in 31 recruits with AD and in 31 control recruits...

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Veröffentlicht in:Japanese journal of radiology 2017-04, Vol.35 (4), p.151-160
Hauptverfasser: Li, Hui, Lin, Yuning, Chen, Ji, Wang, Xiaoyang, Wu, Qingqing, Li, Qi, Chen, Ziqian
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Sprache:eng
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Zusammenfassung:Purpose To explore the regional spontaneous neural activity and functional connectivity alterations of adjustment disorder (AD) in new recruits with in vivo resting-state functional MR (rs-fMRI). Materials and methods Resting-state fMRI was performed in 31 recruits with AD and in 31 control recruits. Regional homogeneity (ReHo) was used to detect the regional synchronizing features of neuronal activations. Correlative analysis was performed to investigate the relationship between the Symptom Check List-90 (SCL-90) score and ReHo in regions with significant group differences. Regions with significant correlation were then defined as regions of interest (ROIs), and seed-ROI based whole-brain functional connectivity was performed. Results Compared with the controls, patients with AD had significantly lower ReHo in the left posterior cerebellar lobe, bilateral medial orbitofrontal cortex, bilateral caudate and left middle temporal gyrus, whereas regions with enhanced ReHo were confined to bilateral posterior cingulate gyrus/precuneus. Only the left posterior cerebellar lobe showed significant correlation between ReHo and the SCL-90 score, and was defined as the seed ROI. Decreased functional connectivity was found between the ROI and bilateral supplementary motor area. Conclusion This study reveals abnormalities in recruits with AD in baseline brain function activities, which could further improve our understanding of the neural substrates of cognitive impairment in AD.
ISSN:1867-1071
1867-108X
DOI:10.1007/s11604-017-0614-2