Abstract

The etiology and maintenance of insomnia are proposed to be associated with increased cognitive and physiological arousal caused by acute stressors and associated cognitive rumination. A core feature of such hyperarousal theory of insomnia involves increased sensory processing that interferes with the onset and maintenance of sleep. In this work, we collected structural magnetic resonance imaging data from 35 patients with primary insomnia and 35 normal sleepers and applied structural covariance analysis to investigate whether insomnia is associated with disruptions in structural brain networks centered at the sensory regions (primary visual, primary auditory, and olfactory cortex). As expected, insomnia patients showed increased structural covariance in cortical thickness between sensory and motor regions. We also observed trends of increased covariance between sensory regions and the default-mode network, and the salience network regions, and trends of decreased covariance between sensory regions and the frontoparietal working memory network regions, in insomnia patients. The observed changes in structural covariance tended to correlated with poor sleep quality. Our findings support previous functional neuroimaging studies and provide novel insights into variations in brain network configuration that may be involved in the pathophysiology of insomnia.

Highlights

  • Chronic insomnia is the most prevalent sleep complaint, which affects about 20% of adult population worldwide [1]

  • Insomnia can be classified as an independent psychiatric syndrome, known as primary insomnia (PI), and a common comorbidity associated with a variety of physical and psychiatric disorders, known as secondary insomnia [10]

  • We explored whether cortical thickness was associated with the sleep quality, measured as PSQI scores, by computing Pearson’s correlation coefficients removing the effects of age, gender, and global mean cortical thickness

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Summary

Introduction

Chronic insomnia is the most prevalent sleep complaint, which affects about 20% of adult population worldwide [1]. Insomnia is associated with reduced quality of life [2], cognitive impairments [3], physical complaints [4], and poor social functioning [5]. Chronic insomnia can increase vulnerability for psychiatric disorders [6, 7] and cardiovascular morbidity and mortality [8] and is associated with increased health care consumption [9]. 25% of the population with chronic insomnia is considered to have PI [11]. Studying chronic PI may allow investigation of the biology of insomnia in a relatively pure condition, independent of influences attributable to any coexisting comorbid medical or psychiatric disorders [12]

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