Abstract

Cortical hyperarousal is higher in insomnia sufferers (INS) than in good sleepers (GS) and could be related to an alteration in sleep protection mechanisms, like reduced density or altered characteristics in sleep spindles. The deficient sleep protection mechanisms might in turn enhance underestimation of sleep. This study's objective was to document sleep spindles characteristics in INS compared with GS and to investigate their potential role in sleep consolidation and misperception. Seventeen individuals with paradoxical insomnia (PARA-I), 24 individuals with psychophysiological insomnia (PSY-I), and 29 GS completed four consecutive polysomnographic nights in laboratory. Sleep spindles were detected automatically during stage 2 and SWS (3-4) on night 3. Number, density, duration, frequency, and amplitude of sleep spindles were calculated. A misperception index was used to determine the degree of discrepancy between subjective and objective total sleep times. Kruskal-Wallis H tests and post hoc tests revealed that PARA-I had significantly shorter sleep spindles than GS but that PSY-I and GS did not differ on spindles length. A standard multiple regression model revealed that neither sleep spindles characteristics nor objective sleep measures were predictive of sleep misperception. A longer duration of spindles could reflect a higher gating process but this hypothesis still needs to be confirmed in replication studies.

Highlights

  • Insomnia is the most prevailing sleep disorder

  • A negative correlation between the probability of nucleus reticularis thalami (nRT) neurons to be involved in the first cycle of sleep spindle and the duration of the spindle was observed in cats [16]

  • Sleep spindles duration in stage 2 differed between paradoxical insomnia (PARA-I) and good sleepers (GS), as the length of spindles is shorter for this insomnia subgroup

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Summary

Introduction

Insomnia is the most prevailing sleep disorder. Approximately 30 to 48% of adults complain of insomnia symptoms [1] and 10% have symptoms significant enough to meet the diagnostic criteria of insomnia syndrome [2]. Even if insomnia sufferers (INS) spend more time in stage 1 and less time in stages 3 and 4 and display more frequent changes in sleep stages [4,5,6], sleep protection mechanisms and their role towards the altered sleep of INS have been scarcely studied. These sleep protection mechanisms might be deficient in INS, impairing sleep soundness. Less sound sleep could be linked to one’s ability to adequately perceive sleep

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