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Related Experiment Video

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Stimulus-specific Cortical Visual Evoked Potential Morphological Patterns

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Published on: May 12, 2019

Abnormal sensory processing cortex in insomnia disorder: a degree centrality study.

Hui Wang^1,2, Haining Li³, Ziyi Liu²

¹School of Future Technology, Xi'an Jiaotong University, Xi'an, 710049, China.

Brain Imaging and Behavior

|January 17, 2025

Summary

Insomnia disorder involves altered brain network centrality, particularly in sensory and emotional processing regions. These brain changes correlate with sleep quality and depression symptoms, offering insights into insomnia

Keywords:

Degree centrality Functional magnetic resonance imaging Insomnia disorder Sensory cortex Thalamus

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Area of Science:

Neuroscience
Medical Imaging
Sleep Medicine

Background:

Insomnia disorder is a prevalent global health issue.
Understanding its pathogenesis is crucial for effective treatment.
Brain network dysfunction is increasingly implicated in insomnia.

Purpose of the Study:

To investigate the pathogenesis of insomnia disorder using voxel-level static and dynamic degree centrality.
To compare brain centrality measures between insomnia patients and healthy controls.
To explore correlations between altered centrality and clinical indicators of insomnia.

Main Methods:

Employed static and dynamic degree centrality analysis at the voxel level.
Included 29 insomnia disorder patients and 28 healthy controls.
Correlated degree centrality values with the Pittsburgh Sleep Quality Index and Hamilton Depression Scale.

Main Results:

Insomnia patients showed higher static degree centrality in sensory processing areas (occipital gyrus, inferior temporal gyrus) and lower centrality in subcortical regions (amygdala, thalamus).
Dynamic degree centrality alterations were observed in the default mode network and salience network regions.
Negative correlation between dynamic centrality (inferior parietal gyrus) and sleep quality; positive correlation between static centrality (inferior temporal gyrus) and depression severity.

Conclusions:

Dysfunctional brain network centrality in sensory and subcortical regions is linked to sleep-wake imbalance in insomnia.
Altered network dynamics in default mode and salience networks contribute to insomnia neuropathogenesis.
Findings support hyperarousal mechanisms and offer novel perspectives on insomnia's neural underpinnings.