Back to Search
Start Over
Examining resting-state functional connectivity in key hubs of the default mode network in chronic low back pain
- Publication Year :
- 2021
-
Abstract
- <jats:title>Abstract</jats:title> <jats:sec id="j_sjpain-2020-0184_abs_001"> <jats:title>Objectives</jats:title> <jats:p>Changes in brain connectivity have been observed within the default mode network (DMN) in chronic low back pain (CLBP), however the extent of these disruptions and how they may be related to CLBP requires further examination. While studies using seed-based analysis have found disrupted functional connectivity in the medial prefrontal cortex (mPFC), a major hub of the DMN, limited studies have investigated other equally important hubs, such as the posterior cingulate cortex (PCC) in CLBP.</jats:p> </jats:sec> <jats:sec id="j_sjpain-2020-0184_abs_002"> <jats:title>Methods</jats:title> <jats:p>This preliminary study comprised 12 individuals with CLBP and 12 healthy controls who completed a resting-state functional magnetic resonance imaging (fMRI) scan. The mPFC and PCC were used as seeds to assess functional connectivity.</jats:p> </jats:sec> <jats:sec id="j_sjpain-2020-0184_abs_003"> <jats:title>Results</jats:title> <jats:p>Both groups displayed similar patterns of DMN connectivity, however group comparisons showed that CLBP group had reduced connectivity between the PCC and angular gyrus compared to healthy controls. An exploratory analysis examined whether the alterations observed in mPFC and PCC connectivity were related to pain catastrophizing in CLBP, but no significant associations were observed.</jats:p> </jats:sec> <jats:sec id="j_sjpain-2020-0184_abs_004"> <jats:title>Conclusions</jats:title> <jats:p>These results may suggest alterations in the PCC are apparent in CLBP, however, the impact and functional role of these disruptions require further investigation.</jats:p> </jats:sec>
Details
- Database :
- OAIster
- Notes :
- 8 p., English
- Publication Type :
- Electronic Resource
- Accession number :
- edsoai.on1269428501
- Document Type :
- Electronic Resource