Aberrantly higher functional connectivity in the salience network is associated with transient global amnesia
Geon Ha Kim1, Bori R Kim1,2, Min Young Chun1
1Department of Neurology, College of Medicine, Ewha Womans University Mokdong Hospital, Ewha Womans University, Seoul, Republic of Korea.
Transient global amnesia (TGA) involves temporary changes in brain network connectivity. Early in TGA, the salience network (SN) shows increased connectivity, while the default mode network (DMN) shows decreased connectivity.
Area of Science:
- Neuroscience
- Cognitive Neuroscience
- Medical Imaging
Background:
- The salience network (SN), default mode network (DMN), and central executive network (CEN) are crucial for human cognition.
- Transient global amnesia (TGA) is a condition characterized by temporary memory loss.
- Understanding TGA's pathophysiology may benefit from examining intrinsic brain networks.
Purpose of the Study:
- To investigate alterations in intrinsic brain networks (SN, DMN, CEN) in patients with TGA.
- To explore the temporal dynamics of these network changes following TGA onset.
Main Methods:
- Resting-state functional magnetic resonance imaging (rsfMRI) was performed on 50 TGA patients and 25 healthy controls.
- rsfMRI scans were acquired within 24 hours, at 72 hours, and 3 months after TGA onset.
- Functional connectivity analysis was conducted on the SN, DMN, and CEN.
Main Results:
- Within 24 hours of TGA onset, patients exhibited increased SN connectivity and decreased DMN connectivity, with preserved CEN connectivity.
- At 72 hours, DMN connectivity remained decreased, while SN connectivity showed no significant alterations.
- By 3 months post-onset, functional connectivity in both SN and DMN returned to normal levels.
Conclusions:
- TGA is associated with transient alterations in intrinsic brain network connectivity, specifically increased SN and decreased DMN connectivity.
- These network changes are temporary and normalize over time.
- The findings offer insights into the neurobiological underpinnings of TGA pathophysiology.
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